β2-adrenergic receptor signaling regulates metabolic pathways critical to myeloid-derived suppressor cell function within the TME

Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrener...

Celý popis

Uloženo v:

Podrobná bibliografie
Vydáno v:	Cell reports (Cambridge) Ročník 37; číslo 4; s. 109883
Hlavní autoři:	Mohammadpour, Hemn, MacDonald, Cameron R., McCarthy, Philip L., Abrams, Scott I., Repasky, Elizabeth A.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 26.10.2021
Témata:	Animals autophagy cancer fatty acid oxidation immune suppression Lipid Metabolism - genetics Lipid Metabolism - immunology MDSCs metabolism Mice Mice, Knockout Myeloid-Derived Suppressor Cells - metabolism Neoplasm Proteins - genetics Neoplasm Proteins - immunology Neoplasms - genetics Neoplasms - immunology Oxidative Phosphorylation prostaglandin E2 Receptors, Adrenergic, beta-2 - genetics Receptors, Adrenergic, beta-2 - immunology Signal Transduction - immunology stress Tumor Microenvironment - genetics Tumor Microenvironment - immunology β-adrenergic signaling stress MDSCs autophagy prostaglandin E2 cancer metabolism β-adrenergic signaling fatty acid oxidation immune suppression oxidative phosphorylation
ISSN:	2211-1247, 2211-1247
On-line přístup:	Získat plný text
Tagy:	Přidat tag Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!

Abstract	Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function. [Display omitted] •Tumor progression increases the expression of β2-AR on MDSCs•β2-AR signaling increases fatty acid oxidation and oxidative phosphorylation in MDSCs•β2-AR signaling in MDSCs increases autophagy-mediated PGE2 production Mohammadpour et al. show that β2-AR signaling in MDSCs alters their metabolic state and increases their immunosuppressive function. Specific processes found to be increased include fatty acid oxidation, oxidative phosphorylation, and autophagy. In addition, these metabolic alterations facilitate an increase in PGE2 production via elevated COX2 expression.
AbstractList	Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function. Mohammadpour et al. show that β2-AR signaling in MDSCs alters their metabolic state and increases their immunosuppressive function. Specific processes found to be increased include fatty acid oxidation, oxidative phosphorylation, and autophagy. In addition, these metabolic alterations facilitate an increase in PGE2 production via elevated COX2 expression. Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function. [Display omitted] •Tumor progression increases the expression of β2-AR on MDSCs•β2-AR signaling increases fatty acid oxidation and oxidative phosphorylation in MDSCs•β2-AR signaling in MDSCs increases autophagy-mediated PGE2 production Mohammadpour et al. show that β2-AR signaling in MDSCs alters their metabolic state and increases their immunosuppressive function. Specific processes found to be increased include fatty acid oxidation, oxidative phosphorylation, and autophagy. In addition, these metabolic alterations facilitate an increase in PGE2 production via elevated COX2 expression. Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function.Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function. Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved. Identifying these mechanisms could lead to therapeutic interventions to boost cancer immunotherapy efficacy. Here, we reveal that β2 adrenergic receptor (β2-AR) expression on MDSCs increases with tumor growth and that the β2-AR stress pathway drives the immune suppressive activity of MDSCs by altering their metabolism. We show that β2-AR signaling decreases glycolysis and increases oxidative phosphorylation and fatty acid oxidation (FAO). It also increases expression of the fatty acid transporter CPT1A, which is necessary for the FAO-mediated immunosuppressive function of MDSCs. Moreover, we show that β2-AR signaling increases autophagy and activates the arachidonic acid cycle, both required for increasing the release of the immunosuppressive mediator, PGE2. Our data reveal that β2-AR signaling triggered by stress is an important physiological regulator of key metabolic pathways in MDSCs, driving their immunosuppressive function.
ArticleNumber	109883
Author	Repasky, Elizabeth A. Abrams, Scott I. MacDonald, Cameron R. McCarthy, Philip L. Mohammadpour, Hemn
AuthorAffiliation	2 Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA 1 Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA 3 Lead contact
AuthorAffiliation_xml	– name: 2 Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA – name: 3 Lead contact – name: 1 Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA
Author_xml	– sequence: 1 givenname: Hemn orcidid: 0000-0002-0158-7283 surname: Mohammadpour fullname: Mohammadpour, Hemn email: hemn.mohammadpour@roswellpark.org organization: Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA – sequence: 2 givenname: Cameron R. orcidid: 0000-0002-7402-7113 surname: MacDonald fullname: MacDonald, Cameron R. organization: Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA – sequence: 3 givenname: Philip L. orcidid: 0000-0002-9577-3879 surname: McCarthy fullname: McCarthy, Philip L. organization: Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA – sequence: 4 givenname: Scott I. orcidid: 0000-0002-8742-4708 surname: Abrams fullname: Abrams, Scott I. organization: Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA – sequence: 5 givenname: Elizabeth A. surname: Repasky fullname: Repasky, Elizabeth A. email: elizabeth.repasky@roswellpark.org organization: Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34706232$$D View this record in MEDLINE/PubMed
BookMark	eNqFUctuFDEQtFAQCSF_gJCPXGaxPc_lgISiQCIFcQlny-Ppme2Vxx5sz0Z7zSfxIXwTHu0GBQ7gi612dVV31UtyYp0FQl5ztuKMV--2Kw3Gw7QSTPBUWjdN_oycCcF5xkVRnzx5n5KLELYsnYpxvi5ekNO8qFklcnFGHn7-EJnqPFjwA2rqQcMUnacBB6sM2iGVhtmoCIGOEFXrTIJNKm7u1T5Q7TGiVoZGR8c9GIdd1oHHHXQ0zNPkIYTElqY1tJ-tjugsvce4QUvjBujdl6tX5HmvTICL431Ovn26uru8zm6_fr65_Hib6aLKY1ZVfalYXyidN02dg2hVUZZlq2tetWvOBe9FXop1CVCyJheNYHUBnNdrXqeqys_JhwPvNLcjdBps9MrIyeOo_F46hfLPH4sbObidbJJvBasSwdsjgXffZwhRjhiWzZQFNwcpyqauqzTTAn3zVOu3yKPxCfD-ANDeheChlxqjWtxJ0mgkZ3IJWm7lIWi5BC0PQafm4q_mR_7_tB0NgOTyDsHLoBGshg5T7FF2Dv9N8Auzy8bh
CitedBy_id	crossref_primary_10_1007_s12032_025_02911_1 crossref_primary_10_1038_s41577_023_00949_8 crossref_primary_10_1245_s10434_024_16195_8 crossref_primary_10_3389_fcell_2024_1310442 crossref_primary_10_1016_j_scib_2025_09_034 crossref_primary_10_3389_fimmu_2024_1497468 crossref_primary_10_1038_s41467_024_47096_9 crossref_primary_10_1111_vco_12891 crossref_primary_10_1177_15347354221096081 crossref_primary_10_3390_futurepharmacol5030038 crossref_primary_10_1016_j_jare_2025_08_052 crossref_primary_10_1186_s40364_024_00646_1 crossref_primary_10_1016_j_breast_2025_104474 crossref_primary_10_1186_s13578_023_01138_9 crossref_primary_10_3390_cells11010020 crossref_primary_10_1016_j_smim_2022_101657 crossref_primary_10_3390_cancers14102541 crossref_primary_10_1002_adbi_202300528 crossref_primary_10_1002_mco2_784 crossref_primary_10_1111_crj_70080 crossref_primary_10_1038_s41419_023_05631_4 crossref_primary_10_1016_j_molmed_2023_05_010 crossref_primary_10_1053_j_gastro_2024_05_014 crossref_primary_10_1002_adbi_202200031 crossref_primary_10_1002_eji_202250345 crossref_primary_10_1136_jitc_2025_011609 crossref_primary_10_1002_ctm2_1483 crossref_primary_10_1016_j_intimp_2025_115321 crossref_primary_10_1016_j_bbrc_2024_150042 crossref_primary_10_1136_jitc_2023_007802 crossref_primary_10_1016_j_biopha_2024_116609 crossref_primary_10_1186_s12943_025_02277_y crossref_primary_10_3390_cancers16010074 crossref_primary_10_1016_j_pharmthera_2025_108849 crossref_primary_10_3389_fcell_2022_896147 crossref_primary_10_3389_fimmu_2022_1102471 crossref_primary_10_1016_j_celrep_2025_116059 crossref_primary_10_1186_s12929_023_00903_9 crossref_primary_10_32604_biocell_2023_027677 crossref_primary_10_32604_or_2024_048564 crossref_primary_10_1016_j_cstres_2024_01_006 crossref_primary_10_1210_endocr_bqad126 crossref_primary_10_1097_CMR_0000000000000943 crossref_primary_10_1007_s11684_025_1124_8 crossref_primary_10_3389_fimmu_2022_842949 crossref_primary_10_1136_jitc_2024_009910 crossref_primary_10_1186_s12943_025_02413_8 crossref_primary_10_1016_j_cophys_2023_100720 crossref_primary_10_3389_fimmu_2025_1653548 crossref_primary_10_1155_2022_8300187 crossref_primary_10_1080_08820139_2023_2232403 crossref_primary_10_3389_fcell_2022_887076 crossref_primary_10_1016_j_bbcan_2025_189447 crossref_primary_10_1038_s41417_025_00886_9 crossref_primary_10_3389_fimmu_2022_1018903 crossref_primary_10_3389_fnins_2023_1321176 crossref_primary_10_3390_cells14070496 crossref_primary_10_3389_fphar_2024_1423502 crossref_primary_10_1186_s12967_025_06657_2 crossref_primary_10_1007_s10549_024_07369_9 crossref_primary_10_1101_gad_352294_124 crossref_primary_10_1038_s41416_022_01891_7 crossref_primary_10_1111_febs_17280 crossref_primary_10_3390_ijms24010767 crossref_primary_10_1038_s41392_025_02241_8 crossref_primary_10_3389_fimmu_2023_1141712 crossref_primary_10_3390_biology13110949 crossref_primary_10_3389_fimmu_2022_937406 crossref_primary_10_1016_j_canlet_2025_217451 crossref_primary_10_1016_j_canlet_2024_217076 crossref_primary_10_1158_2326_6066_CIR_23_0976 crossref_primary_10_3389_fimmu_2022_933847 crossref_primary_10_1186_s10020_025_01132_6 crossref_primary_10_1186_s12943_024_02219_0 crossref_primary_10_1038_s41568_025_00831_w
Cites_doi	10.1189/jlb.1209821 10.1038/ncomms14979 10.1038/s41590-017-0022-x 10.3389/fimmu.2018.00398 10.1007/s00281-020-00815-y 10.1158/2326-6066.CIR-20-0445 10.1172/JCI129502 10.1188/20.CJON.51-57 10.1126/sciimmunol.aay6017 10.1016/j.it.2016.01.004 10.1158/2159-8290.CD-18-1398 10.1080/2162402X.2017.1405205 10.1172/JCI120888 10.1189/jlb.0510303 10.1158/2326-6066.CIR-15-0036 10.3389/fimmu.2019.00475 10.1042/CS20060307 10.1038/cddis.2016.132 10.1038/ni.1937 10.1172/JCI97953 10.3389/fimmu.2019.01399 10.4049/jimmunol.1701019 10.1038/s41416-019-0650-z 10.1007/s00281-012-0342-8 10.1016/j.immuni.2015.09.001 10.1038/s41419-020-02936-6 10.1038/s41593-019-0430-3 10.1189/jlb.3HI0715-305R 10.1038/jid.2015.3 10.1038/s41577-020-00490-y 10.1016/j.it.2014.12.005 10.1155/2019/3809308 10.1016/j.cellimm.2021.104297 10.1126/science.1236361 10.1186/1471-2121-13-18 10.1016/j.cmet.2018.04.022 10.1073/pnas.1304291110 10.1007/s00262-018-2243-8 10.1158/0008-5472.CAN-06-4174 10.4103/1673-5374.244793 10.1158/0008-5472.CAN-17-0546 10.1038/s41416-019-0644-x 10.3389/fimmu.2019.00115 10.1038/s41467-020-17882-2 10.1016/j.cmet.2006.05.011 10.1080/2162402X.2017.1344804 10.1038/s41416-018-0333-1 10.1073/pnas.1306340110 10.1016/j.jnutbio.2015.11.002 10.1096/fj.201801733R 10.3389/fimmu.2020.01371 10.1158/1078-0432.CCR-20-2381 10.15698/cst2019.02.176 10.1093/nar/gkw377 10.3389/fimmu.2019.00172 10.1038/s41586-019-1118-2 10.1111/imr.12655 10.1016/j.pharmthera.2006.11.006
ContentType	Journal Article
Copyright	2021 The Author(s) Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
Copyright_xml	– notice: 2021 The Author(s) – notice: Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
DBID	6I. AAFTH AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM
DOI	10.1016/j.celrep.2021.109883
DatabaseName	ScienceDirect Open Access Titles Elsevier:ScienceDirect:Open Access CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles)
DatabaseTitle	CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic MEDLINE
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Biology
EISSN	2211-1247
EndPage	109883
ExternalDocumentID	PMC8601406 34706232 10_1016_j_celrep_2021_109883 S221112472101353X
Genre	Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural
GrantInformation_xml	– fundername: NCI NIH HHS grantid: R01 CA205246 – fundername: NCI NIH HHS grantid: F32 CA239356 – fundername: NCI NIH HHS grantid: R01 CA172105 – fundername: NCI NIH HHS grantid: T32 CA085183 – fundername: NHLBI NIH HHS grantid: K99 HL155792 – fundername: NCI NIH HHS grantid: R01 CA099326 – fundername: NCI NIH HHS grantid: P30 CA016056 – fundername: NCI NIH HHS grantid: F30 CA265127
GroupedDBID	0R~ 0SF 4.4 457 53G 5VS 6I. AACTN AAEDT AAEDW AAFTH AAIKJ AAKRW AALRI AAUCE AAXUO ABMAC ABMWF ACGFO ACGFS ADBBV ADEZE AENEX AEXQZ AFTJW AGHFR AITUG ALKID ALMA_UNASSIGNED_HOLDINGS AMRAJ BAWUL BCNDV DIK EBS EJD FCP FDB FRP GROUPED_DOAJ GX1 IXB KQ8 M41 M48 NCXOZ O-L O9- OK1 RCE ROL SSZ AAMRU AAYWO AAYXX ACVFH ADCNI ADVLN AEUPX AFPUW AIGII AKBMS AKRWK AKYEP APXCP CITATION HZ~ IPNFZ RIG CGR CUY CVF ECM EIF NPM 7X8 5PM
ID	FETCH-LOGICAL-c463t-66f5a0f4ac38873e2ba4555bc716b91121f235295ee5083282074e117917295a3
ISICitedReferencesCount	87
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000711887800003&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	2211-1247
IngestDate	Tue Sep 30 17:04:15 EDT 2025 Wed Oct 01 14:49:47 EDT 2025 Thu Jan 02 22:55:16 EST 2025 Wed Nov 05 20:54:18 EST 2025 Tue Nov 18 21:35:26 EST 2025 Tue Jul 25 21:02:19 EDT 2023
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	4
Keywords	stress MDSCs autophagy prostaglandin E2 cancer metabolism β-adrenergic signaling fatty acid oxidation immune suppression oxidative phosphorylation
Language	English
License	This is an open access article under the CC BY-NC-ND license. Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
LinkModel	OpenURL
MergedId	FETCHMERGED-LOGICAL-c463t-66f5a0f4ac38873e2ba4555bc716b91121f235295ee5083282074e117917295a3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 H.M. initiated and H.M., C.R.M., S.I.A., and E.A.R. designed the study; H.M. performed the experiments, with assistance from C.R.M. H.M., C.R.M., P.L.M., S.I.A., and E.A.R. analyzed and interpreted the data and wrote the paper. AUTHOR CONTRIBUTIONS
ORCID	0000-0002-8742-4708 0000-0002-0158-7283 0000-0002-9577-3879 0000-0002-7402-7113
OpenAccessLink	http://dx.doi.org/10.1016/j.celrep.2021.109883
PMID	34706232
PQID	2587765556
PQPubID	23479
PageCount	1
ParticipantIDs	pubmedcentral_primary_oai_pubmedcentral_nih_gov_8601406 proquest_miscellaneous_2587765556 pubmed_primary_34706232 crossref_citationtrail_10_1016_j_celrep_2021_109883 crossref_primary_10_1016_j_celrep_2021_109883 elsevier_sciencedirect_doi_10_1016_j_celrep_2021_109883
PublicationCentury	2000
PublicationDate	2021-10-26
PublicationDateYYYYMMDD	2021-10-26
PublicationDate_xml	– month: 10 year: 2021 text: 2021-10-26 day: 26
PublicationDecade	2020
PublicationPlace	United States
PublicationPlace_xml	– name: United States
PublicationTitle	Cell reports (Cambridge)
PublicationTitleAlternate	Cell Rep
PublicationYear	2021
Publisher	Elsevier Inc
Publisher_xml	– name: Elsevier Inc
References	Qiao, Chen, Mohammadpour, MacDonald, Bucsek, Hylander, Barbi, Repasky (bib40) 2021; 9 Raud, McGuire, Jones, Sparwasser, Berod (bib43) 2018; 283 Li, Tanikawa, Kryczek, Xia, Li, Wu, Wei, Zhao, Vatan, Wen (bib28) 2018; 28 Yan, Adeshakin, Xu, Afolabi, Zhang, Chen, Wan (bib57) 2019; 10 Kokolus, Capitano, Lee, Eng, Waight, Hylander, Sexton, Hong, Gordon, Abrams, Repasky (bib23) 2013; 110 Kuleshov, Jones, Rouillard, Fernandez, Duan, Wang, Koplev, Jenkins, Jagodnik, Lachmann (bib26) 2016; 44 Alissafi, Hatzioannou, Mintzas, Barouni, Banos, Sormendi, Polyzos, Xilouri, Wielockx, Gogas, Verginis (bib3) 2018; 128 Gandhi, Pandey, Attwood, Ji, Witkiewicz, Knudsen, Allen, Tario, Wallace, Cedeno (bib13) 2021; 27 Veglia, Tyurin, Blasi, De Leo, Kossenkov, Donthireddy, To, Schug, Basu, Wang (bib50) 2019; 569 Vats, Mukundan, Odegaard, Zhang, Smith, Morel, Wagner, Greaves, Murray, Chawla (bib48) 2006; 4 Qiao, Bucsek, Winder, Chen, Giridharan, Olejniczak, Hylander, Repasky (bib39) 2019; 68 Won, Deshane, Leavenworth, Oliva, Griguer (bib55) 2019; 3 Groth, Hu, Weber, Fleming, Altevogt, Utikal, Umansky (bib15) 2019; 120 Kokolus, Zhang, Sivik, Schmeck, Zhu, Repasky, Drabick, Schell (bib24) 2017; 7 Nakanishi, Rosenberg (bib33) 2013; 35 Ramos, Arnsten (bib42) 2007; 113 Hammami, Chen, Murschel, Bronte, De Crescenzo, Jolicoeur (bib16) 2012; 13 Wang, DuBois (bib53) 2018; 128 Roca-Agujetas, de Dios, Lestón, Marí, Morales, Colell (bib44) 2019; 2019 Al-Khami, Zheng, Del Valle, Hossain, Wyczechowska, Zabaleta, Sanchez, Dean, Rodriguez, Ochoa (bib2) 2017; 6 Bucsek, Qiao, MacDonald, Giridharan, Evans, Niedzwecki, Liu, Kokolus, Eng, Messmer (bib8) 2017; 77 Pawelec, Picard, Bueno, Verschoor, Ostrand-Rosenberg (bib38) 2021; 362 Wang, Ding, Guo, Wang (bib54) 2019; 10 Ouzounova, Lee, Piranlioglu, El Andaloussi, Kolhe, Demirci, Marasco, Asm, Chadli, Hassan (bib36) 2017; 8 Lochner, Berod, Sparwasser (bib29) 2015; 36 Tomić, Joksimović, Bekić, Vasiljević, Milanović, Čolić, Vučević (bib47) 2019; 10 Magnon, Hall, Lin, Xue, Gerber, Freedland, Frenette (bib30) 2013; 341 Gosain, Gage-Bouchard, Ambrosone, Repasky, Gandhi (bib14) 2020; 42 Hubler, Kennedy (bib21) 2016; 34 Alshetaiwi, Pervolarakis, McIntyre, Ma, Nguyen, Rath, Nee, Hernandez, Evans, Torosian (bib4) 2020; 5 Bosc, Broin, Fanjul, Saland, Farge, Courdy, Batut, Masoud, Larrue, Skuli (bib7) 2020; 11 Cluxton, Petrasca, Moran, Fletcher (bib9) 2019; 10 He, Ren, Guo, Deng (bib17) 2019; 14 Veglia, Perego, Gabrilovich (bib49) 2018; 19 Kamiya, Hayama, Kato, Shimomura, Shimomura, Irie, Kaneko, Yanagawa, Kobayashi, Ochiya (bib22) 2019; 22 Holubarsch, Rohrbach, Karrasch, Boehm, Polonski, Ponikowski, Rhein (bib18) 2007; 113 Xiong, Wen, Fairchild, Zaytseva, Weiss, Evers, Gao (bib56) 2020; 11 Biswas (bib5) 2015; 43 Ou, Shi, Dong, Liu, Schmidt, Nagarkatti, Nagarkatti, Fan, Ai (bib35) 2015; 135 Abuatiq, Brown, Wolles, Randall (bib1) 2020; 24 Hossain, Al-Khami, Wyczechowska, Hernandez, Zheng, Reiss, Valle, Trillo-Tinoco, Maj, Zou (bib19) 2015; 3 Ostrand-Rosenberg, Fenselau (bib34) 2018; 200 Biswas, Mantovani (bib6) 2010; 11 Yang, Li, Liu, Dai, Bazhin (bib58) 2020; 11 Hu, Pang, Lin, Zhen, Yi (bib20) 2020; 122 Mohammadpour, MacDonald, Qiao, Chen, Dong, Hylander, McCarthy, Abrams, Repasky (bib31) 2019; 129 Serafini (bib45) 2010; 88 Nachmany, Bogoch, Sivan, Amar, Bondar, Zohar, Yakubovsky, Fainaru, Klausner, Pencovich (bib32) 2019; 33 Faulkner, Jobling, March, Jiang, Hondermarck (bib11) 2019; 9 Vistein, Puthenveedu (bib52) 2013; 110 Parker, Horn, Ostrand-Rosenberg (bib37) 2016; 100 Koundouros, Poulogiannis (bib25) 2020; 122 Eruslanov, Daurkin, Ortiz, Vieweg, Kusmartsev (bib10) 2010; 88 Veglia, Sanseviero, Gabrilovich (bib51) 2021; 21 Sinha, Clements, Fulton, Ostrand-Rosenberg (bib46) 2007; 67 Kumar, Patel, Tcyganov, Gabrilovich (bib27) 2016; 37 Qu, Zeng, Liu, Wang, Deng (bib41) 2016; 7 Fleming, Hu, Weber, Nagibin, Groth, Altevogt, Utikal, Umansky (bib12) 2018; 9 Bucsek (10.1016/j.celrep.2021.109883_bib8) 2017; 77 Gosain (10.1016/j.celrep.2021.109883_bib14) 2020; 42 Hossain (10.1016/j.celrep.2021.109883_bib19) 2015; 3 Qu (10.1016/j.celrep.2021.109883_bib41) 2016; 7 Roca-Agujetas (10.1016/j.celrep.2021.109883_bib44) 2019; 2019 Tomić (10.1016/j.celrep.2021.109883_bib47) 2019; 10 Hammami (10.1016/j.celrep.2021.109883_bib16) 2012; 13 Al-Khami (10.1016/j.celrep.2021.109883_bib2) 2017; 6 Kokolus (10.1016/j.celrep.2021.109883_bib24) 2017; 7 Alshetaiwi (10.1016/j.celrep.2021.109883_bib4) 2020; 5 Won (10.1016/j.celrep.2021.109883_bib55) 2019; 3 Bosc (10.1016/j.celrep.2021.109883_bib7) 2020; 11 Nakanishi (10.1016/j.celrep.2021.109883_bib33) 2013; 35 Vistein (10.1016/j.celrep.2021.109883_bib52) 2013; 110 Sinha (10.1016/j.celrep.2021.109883_bib46) 2007; 67 Kokolus (10.1016/j.celrep.2021.109883_bib23) 2013; 110 Veglia (10.1016/j.celrep.2021.109883_bib49) 2018; 19 Cluxton (10.1016/j.celrep.2021.109883_bib9) 2019; 10 Magnon (10.1016/j.celrep.2021.109883_bib30) 2013; 341 Eruslanov (10.1016/j.celrep.2021.109883_bib10) 2010; 88 Kamiya (10.1016/j.celrep.2021.109883_bib22) 2019; 22 Fleming (10.1016/j.celrep.2021.109883_bib12) 2018; 9 He (10.1016/j.celrep.2021.109883_bib17) 2019; 14 Hu (10.1016/j.celrep.2021.109883_bib20) 2020; 122 Wang (10.1016/j.celrep.2021.109883_bib53) 2018; 128 Faulkner (10.1016/j.celrep.2021.109883_bib11) 2019; 9 Biswas (10.1016/j.celrep.2021.109883_bib5) 2015; 43 Mohammadpour (10.1016/j.celrep.2021.109883_bib31) 2019; 129 Ouzounova (10.1016/j.celrep.2021.109883_bib36) 2017; 8 Koundouros (10.1016/j.celrep.2021.109883_bib25) 2020; 122 Lochner (10.1016/j.celrep.2021.109883_bib29) 2015; 36 Raud (10.1016/j.celrep.2021.109883_bib43) 2018; 283 Serafini (10.1016/j.celrep.2021.109883_bib45) 2010; 88 Biswas (10.1016/j.celrep.2021.109883_bib6) 2010; 11 Nachmany (10.1016/j.celrep.2021.109883_bib32) 2019; 33 Li (10.1016/j.celrep.2021.109883_bib28) 2018; 28 Ramos (10.1016/j.celrep.2021.109883_bib42) 2007; 113 Yang (10.1016/j.celrep.2021.109883_bib58) 2020; 11 Pawelec (10.1016/j.celrep.2021.109883_bib38) 2021; 362 Qiao (10.1016/j.celrep.2021.109883_bib39) 2019; 68 Abuatiq (10.1016/j.celrep.2021.109883_bib1) 2020; 24 Yan (10.1016/j.celrep.2021.109883_bib57) 2019; 10 Groth (10.1016/j.celrep.2021.109883_bib15) 2019; 120 Veglia (10.1016/j.celrep.2021.109883_bib51) 2021; 21 Kuleshov (10.1016/j.celrep.2021.109883_bib26) 2016; 44 Qiao (10.1016/j.celrep.2021.109883_bib40) 2021; 9 Ostrand-Rosenberg (10.1016/j.celrep.2021.109883_bib34) 2018; 200 Xiong (10.1016/j.celrep.2021.109883_bib56) 2020; 11 Vats (10.1016/j.celrep.2021.109883_bib48) 2006; 4 Alissafi (10.1016/j.celrep.2021.109883_bib3) 2018; 128 Ou (10.1016/j.celrep.2021.109883_bib35) 2015; 135 Kumar (10.1016/j.celrep.2021.109883_bib27) 2016; 37 Wang (10.1016/j.celrep.2021.109883_bib54) 2019; 10 Veglia (10.1016/j.celrep.2021.109883_bib50) 2019; 569 Gandhi (10.1016/j.celrep.2021.109883_bib13) 2021; 27 Parker (10.1016/j.celrep.2021.109883_bib37) 2016; 100 Holubarsch (10.1016/j.celrep.2021.109883_bib18) 2007; 113 Hubler (10.1016/j.celrep.2021.109883_bib21) 2016; 34
References_xml	– volume: 9 start-page: 398 year: 2018 ident: bib12 article-title: Targeting myeloid-derived suppressor cells to bypass tumor-induced immunosuppression publication-title: Front. Immunol. – volume: 122 start-page: 4 year: 2020 end-page: 22 ident: bib25 article-title: Reprogramming of fatty acid metabolism in cancer publication-title: Br. J. Cancer – volume: 128 start-page: 2732 year: 2018 end-page: 2742 ident: bib53 article-title: Role of prostanoids in gastrointestinal cancer publication-title: J. Clin. Invest. – volume: 34 start-page: 1 year: 2016 end-page: 7 ident: bib21 article-title: Role of lipids in the metabolism and activation of immune cells publication-title: J. Nutr. Biochem. – volume: 77 start-page: 5639 year: 2017 end-page: 5651 ident: bib8 article-title: β-adrenergic signaling in mice housed at standard temperatures suppresses an effector phenotype in CD8+ T cells and undermines checkpoint inhibitor therapy publication-title: Cancer Res. – volume: 36 start-page: 81 year: 2015 end-page: 91 ident: bib29 article-title: Fatty acid metabolism in the regulation of T cell function publication-title: Trends Immunol. – volume: 113 start-page: 523 year: 2007 end-page: 536 ident: bib42 article-title: Adrenergic pharmacology and cognition: focus on the prefrontal cortex publication-title: Pharmacol. Ther. – volume: 68 start-page: 11 year: 2019 end-page: 22 ident: bib39 article-title: β-Adrenergic signaling blocks murine CD8 publication-title: Cancer Immunol. Immunother. – volume: 88 start-page: 827 year: 2010 end-page: 829 ident: bib45 article-title: Editorial: PGE2-producing MDSC: a role in tumor progression? publication-title: J. Leukoc. Biol. – volume: 7 start-page: e1405205 year: 2017 ident: bib24 article-title: Beta blocker use correlates with better overall survival in metastatic melanoma patients and improves the efficacy of immunotherapies in mice publication-title: OncoImmunology – volume: 22 start-page: 1289 year: 2019 end-page: 1305 ident: bib22 article-title: Genetic manipulation of autonomic nerve fiber innervation and activity and its effect on breast cancer progression publication-title: Nat. Neurosci. – volume: 33 start-page: 5967 year: 2019 end-page: 5978 ident: bib32 article-title: CD11b publication-title: FASEB J. – volume: 100 start-page: 463 year: 2016 end-page: 470 ident: bib37 article-title: High-mobility group box protein 1 promotes the survival of myeloid-derived suppressor cells by inducing autophagy publication-title: J. Leukoc. Biol. – volume: 3 start-page: 47 year: 2019 end-page: 65 ident: bib55 article-title: Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma publication-title: Cell Stress – volume: 8 start-page: 14979 year: 2017 ident: bib36 article-title: Monocytic and granulocytic myeloid derived suppressor cells differentially regulate spatiotemporal tumour plasticity during metastatic cascade publication-title: Nat. Commun. – volume: 24 start-page: 51 year: 2020 end-page: 57 ident: bib1 article-title: Perceptions of stress: patient and caregiver experiences with stressors during hospitalization publication-title: Clin. J. Oncol. Nurs. – volume: 35 start-page: 123 year: 2013 end-page: 137 ident: bib33 article-title: Multifaceted roles of PGE 2 in inflammation and cancer publication-title: Semin. Immunopathol. – volume: 10 start-page: 1399 year: 2019 ident: bib57 article-title: Lipid metabolic pathways confer the immunosuppressive function of myeloid-derived suppressor cells in tumor publication-title: Front. Immunol. – volume: 200 start-page: 422 year: 2018 end-page: 431 ident: bib34 article-title: Myeloid-derived suppressor cells: immune-suppressive cells that impair antitumor immunity and are sculpted by their environment publication-title: J. Immunol. – volume: 110 start-page: 15289 year: 2013 end-page: 15294 ident: bib52 article-title: Reprogramming of G protein-coupled receptor recycling and signaling by a kinase switch publication-title: Proc. Natl. Acad. Sci. USA – volume: 44 start-page: W90 year: 2016 end-page: W97 ident: bib26 article-title: Enrichr: a comprehensive gene set enrichment analysis web server 2016 update publication-title: Nucleic Acids Res. – volume: 362 start-page: 104297 year: 2021 ident: bib38 article-title: MDSCs, ageing and inflammageing publication-title: Cell. Immunol. – volume: 14 start-page: 280 year: 2019 end-page: 288 ident: bib17 article-title: Neuronal autophagy aggravates microglial inflammatory injury by downregulating CX3CL1/fractalkine after ischemic stroke publication-title: Neural Regen. Res. – volume: 10 start-page: 115 year: 2019 ident: bib9 article-title: Differential regulation of human Treg and Th17 cells by fatty acid synthesis and glycolysis publication-title: Front. Immunol. – volume: 122 start-page: 23 year: 2020 end-page: 29 ident: bib20 article-title: Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells publication-title: Br. J. Cancer – volume: 7 start-page: e2226 year: 2016 ident: bib41 article-title: Fatty acid oxidation and carnitine palmitoyltransferase I: emerging therapeutic targets in cancer publication-title: Cell Death Dis. – volume: 37 start-page: 208 year: 2016 end-page: 220 ident: bib27 article-title: The nature of myeloid-derived suppressor cells in the tumor microenvironment publication-title: Trends Immunol. – volume: 5 start-page: eaay6017 year: 2020 ident: bib4 article-title: Defining the emergence of myeloid-derived suppressor cells in breast cancer using single-cell transcriptomics publication-title: Sci. Immunol. – volume: 43 start-page: 435 year: 2015 end-page: 449 ident: bib5 article-title: Metabolic reprogramming of immune cells in cancer progression publication-title: Immunity – volume: 113 start-page: 205 year: 2007 end-page: 212 ident: bib18 article-title: A double-blind randomized multicentre clinical trial to evaluate the efficacy and safety of two doses of etomoxir in comparison with placebo in patients with moderate congestive heart failure: the ERGO (etomoxir for the recovery of glucose oxidation) study publication-title: Clin. Sci. (Lond.) – volume: 283 start-page: 213 year: 2018 end-page: 231 ident: bib43 article-title: Fatty acid metabolism in CD8 publication-title: Immunol. Rev. – volume: 21 start-page: 485 year: 2021 end-page: 498 ident: bib51 article-title: Myeloid-derived suppressor cells in the era of increasing myeloid cell diversity publication-title: Nat. Rev. Immunol. – volume: 10 start-page: 172 year: 2019 ident: bib54 article-title: MDSCs: Key Criminals of Tumor Pre-metastatic Niche Formation publication-title: Front. Immunol. – volume: 11 start-page: 736 year: 2020 ident: bib56 article-title: Upregulation of CPT1A is essential for the tumor-promoting effect of adipocytes in colon cancer publication-title: Cell Death Dis. – volume: 11 start-page: 4056 year: 2020 ident: bib7 article-title: Autophagy regulates fatty acid availability for oxidative phosphorylation through mitochondria-endoplasmic reticulum contact sites publication-title: Nat. Commun. – volume: 88 start-page: 839 year: 2010 end-page: 848 ident: bib10 article-title: Pivotal advance: tumor-mediated induction of myeloid-derived suppressor cells and M2-polarized macrophages by altering intracellular PGE publication-title: J. Leukoc. Biol. – volume: 4 start-page: 13 year: 2006 end-page: 24 ident: bib48 article-title: Oxidative metabolism and PGC-1β attenuate macrophage-mediated inflammation publication-title: Cell Metab. – volume: 67 start-page: 4507 year: 2007 end-page: 4513 ident: bib46 article-title: Prostaglandin E2 promotes tumor progression by inducing myeloid-derived suppressor cells publication-title: Cancer Res. – volume: 19 start-page: 108 year: 2018 end-page: 119 ident: bib49 article-title: Myeloid-derived suppressor cells coming of age publication-title: Nat. Immunol. – volume: 6 start-page: e1344804 year: 2017 ident: bib2 article-title: Exogenous lipid uptake induces metabolic and functional reprogramming of tumor-associated myeloid-derived suppressor cells publication-title: OncoImmunology – volume: 27 start-page: 87 year: 2021 end-page: 95 ident: bib13 article-title: Phase I Clinical Trial of Combination Propranolol and Pembrolizumab in Locally Advanced and Metastatic Melanoma: Safety, Tolerability, and Preliminary Evidence of Antitumor Activity publication-title: Clin. Cancer Res. – volume: 110 start-page: 20176 year: 2013 end-page: 20181 ident: bib23 article-title: Baseline tumor growth and immune control in laboratory mice are significantly influenced by subthermoneutral housing temperature publication-title: Proc. Natl. Acad. Sci. USA – volume: 120 start-page: 16 year: 2019 end-page: 25 ident: bib15 article-title: Immunosuppression mediated by myeloid-derived suppressor cells (MDSCs) during tumour progression publication-title: Br. J. Cancer – volume: 135 start-page: 1425 year: 2015 end-page: 1434 ident: bib35 article-title: Kruppel-like factor KLF4 facilitates cutaneous wound healing by promoting fibrocyte generation from myeloid-derived suppressor cells publication-title: J. Invest. Dermatol. – volume: 2019 start-page: 3809308 year: 2019 ident: bib44 article-title: Recent insights into the mitochondrial role in autophagy and its regulation by oxidative stress publication-title: Oxid. Med. Cell. Longev. – volume: 13 start-page: 18 year: 2012 ident: bib16 article-title: Immunosuppressive activity enhances central carbon metabolism and bioenergetics in myeloid-derived suppressor cells in vitro models publication-title: BMC Cell Biol. – volume: 129 start-page: 5537 year: 2019 end-page: 5552 ident: bib31 article-title: β2 adrenergic receptor-mediated signaling regulates the immunosuppressive potential of myeloid-derived suppressor cells publication-title: J. Clin. Invest. – volume: 11 start-page: 1371 year: 2020 ident: bib58 article-title: Myeloid-Derived Suppressor Cells in Tumors: From Mechanisms to Antigen Specificity and Microenvironmental Regulation publication-title: Front. Immunol. – volume: 28 start-page: 87 year: 2018 end-page: 103.e6 ident: bib28 article-title: Aerobic glycolysis controls myeloid-derived suppressor cells and tumor immunity via a specific CEBPB isoform in triple-negative breast cancer publication-title: Cell Metab. – volume: 3 start-page: 1236 year: 2015 end-page: 1247 ident: bib19 article-title: Inhibition of fatty acid oxidation modulates immunosuppressive functions of myeloid-derived suppressor cells and enhances cancer therapies publication-title: Cancer Immunol. Res. – volume: 341 start-page: 1236361 year: 2013 ident: bib30 article-title: Autonomic nerve development contributes to prostate cancer progression publication-title: Science – volume: 10 start-page: 475 year: 2019 ident: bib47 article-title: Prostaglanin-E2 potentiates the suppressive functions of human mononuclear myeloid-derived suppressor cells and increases their capacity to expand IL-10-producing regulatory T cell subsets publication-title: Front. Immunol. – volume: 42 start-page: 719 year: 2020 end-page: 734 ident: bib14 article-title: Stress reduction strategies in breast cancer: review of pharmacologic and non-pharmacologic based strategies publication-title: Semin. Immunopathol. – volume: 128 start-page: 3840 year: 2018 end-page: 3852 ident: bib3 article-title: Autophagy orchestrates the regulatory program of tumor-associated myeloid-derived suppressor cells publication-title: J. Clin. Invest. – volume: 569 start-page: 73 year: 2019 end-page: 78 ident: bib50 article-title: Fatty acid transport protein 2 reprograms neutrophils in cancer publication-title: Nature – volume: 11 start-page: 889 year: 2010 end-page: 896 ident: bib6 article-title: Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm publication-title: Nat. Immunol. – volume: 9 start-page: 651 year: 2021 end-page: 664 ident: bib40 article-title: Chronic Adrenergic Stress Contributes to Metabolic Dysfunction and an Exhausted Phenotype in T Cells in the Tumor Microenvironment publication-title: Cancer Immunol. Res. – volume: 9 start-page: 702 year: 2019 end-page: 710 ident: bib11 article-title: Tumor neurobiology and the war of nerves in cancer publication-title: Cancer Discov. – volume: 88 start-page: 839 year: 2010 ident: 10.1016/j.celrep.2021.109883_bib10 article-title: Pivotal advance: tumor-mediated induction of myeloid-derived suppressor cells and M2-polarized macrophages by altering intracellular PGE2 catabolism in myeloid cells publication-title: J. Leukoc. Biol. doi: 10.1189/jlb.1209821 – volume: 8 start-page: 14979 year: 2017 ident: 10.1016/j.celrep.2021.109883_bib36 article-title: Monocytic and granulocytic myeloid derived suppressor cells differentially regulate spatiotemporal tumour plasticity during metastatic cascade publication-title: Nat. Commun. doi: 10.1038/ncomms14979 – volume: 19 start-page: 108 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib49 article-title: Myeloid-derived suppressor cells coming of age publication-title: Nat. Immunol. doi: 10.1038/s41590-017-0022-x – volume: 9 start-page: 398 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib12 article-title: Targeting myeloid-derived suppressor cells to bypass tumor-induced immunosuppression publication-title: Front. Immunol. doi: 10.3389/fimmu.2018.00398 – volume: 42 start-page: 719 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib14 article-title: Stress reduction strategies in breast cancer: review of pharmacologic and non-pharmacologic based strategies publication-title: Semin. Immunopathol. doi: 10.1007/s00281-020-00815-y – volume: 9 start-page: 651 year: 2021 ident: 10.1016/j.celrep.2021.109883_bib40 article-title: Chronic Adrenergic Stress Contributes to Metabolic Dysfunction and an Exhausted Phenotype in T Cells in the Tumor Microenvironment publication-title: Cancer Immunol. Res. doi: 10.1158/2326-6066.CIR-20-0445 – volume: 129 start-page: 5537 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib31 article-title: β2 adrenergic receptor-mediated signaling regulates the immunosuppressive potential of myeloid-derived suppressor cells publication-title: J. Clin. Invest. doi: 10.1172/JCI129502 – volume: 24 start-page: 51 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib1 article-title: Perceptions of stress: patient and caregiver experiences with stressors during hospitalization publication-title: Clin. J. Oncol. Nurs. doi: 10.1188/20.CJON.51-57 – volume: 5 start-page: eaay6017 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib4 article-title: Defining the emergence of myeloid-derived suppressor cells in breast cancer using single-cell transcriptomics publication-title: Sci. Immunol. doi: 10.1126/sciimmunol.aay6017 – volume: 37 start-page: 208 year: 2016 ident: 10.1016/j.celrep.2021.109883_bib27 article-title: The nature of myeloid-derived suppressor cells in the tumor microenvironment publication-title: Trends Immunol. doi: 10.1016/j.it.2016.01.004 – volume: 9 start-page: 702 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib11 article-title: Tumor neurobiology and the war of nerves in cancer publication-title: Cancer Discov. doi: 10.1158/2159-8290.CD-18-1398 – volume: 7 start-page: e1405205 year: 2017 ident: 10.1016/j.celrep.2021.109883_bib24 article-title: Beta blocker use correlates with better overall survival in metastatic melanoma patients and improves the efficacy of immunotherapies in mice publication-title: OncoImmunology doi: 10.1080/2162402X.2017.1405205 – volume: 128 start-page: 3840 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib3 article-title: Autophagy orchestrates the regulatory program of tumor-associated myeloid-derived suppressor cells publication-title: J. Clin. Invest. doi: 10.1172/JCI120888 – volume: 88 start-page: 827 year: 2010 ident: 10.1016/j.celrep.2021.109883_bib45 article-title: Editorial: PGE2-producing MDSC: a role in tumor progression? publication-title: J. Leukoc. Biol. doi: 10.1189/jlb.0510303 – volume: 3 start-page: 1236 year: 2015 ident: 10.1016/j.celrep.2021.109883_bib19 article-title: Inhibition of fatty acid oxidation modulates immunosuppressive functions of myeloid-derived suppressor cells and enhances cancer therapies publication-title: Cancer Immunol. Res. doi: 10.1158/2326-6066.CIR-15-0036 – volume: 10 start-page: 475 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib47 article-title: Prostaglanin-E2 potentiates the suppressive functions of human mononuclear myeloid-derived suppressor cells and increases their capacity to expand IL-10-producing regulatory T cell subsets publication-title: Front. Immunol. doi: 10.3389/fimmu.2019.00475 – volume: 113 start-page: 205 year: 2007 ident: 10.1016/j.celrep.2021.109883_bib18 article-title: A double-blind randomized multicentre clinical trial to evaluate the efficacy and safety of two doses of etomoxir in comparison with placebo in patients with moderate congestive heart failure: the ERGO (etomoxir for the recovery of glucose oxidation) study publication-title: Clin. Sci. (Lond.) doi: 10.1042/CS20060307 – volume: 7 start-page: e2226 year: 2016 ident: 10.1016/j.celrep.2021.109883_bib41 article-title: Fatty acid oxidation and carnitine palmitoyltransferase I: emerging therapeutic targets in cancer publication-title: Cell Death Dis. doi: 10.1038/cddis.2016.132 – volume: 11 start-page: 889 year: 2010 ident: 10.1016/j.celrep.2021.109883_bib6 article-title: Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm publication-title: Nat. Immunol. doi: 10.1038/ni.1937 – volume: 128 start-page: 2732 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib53 article-title: Role of prostanoids in gastrointestinal cancer publication-title: J. Clin. Invest. doi: 10.1172/JCI97953 – volume: 10 start-page: 1399 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib57 article-title: Lipid metabolic pathways confer the immunosuppressive function of myeloid-derived suppressor cells in tumor publication-title: Front. Immunol. doi: 10.3389/fimmu.2019.01399 – volume: 200 start-page: 422 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib34 article-title: Myeloid-derived suppressor cells: immune-suppressive cells that impair antitumor immunity and are sculpted by their environment publication-title: J. Immunol. doi: 10.4049/jimmunol.1701019 – volume: 122 start-page: 4 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib25 article-title: Reprogramming of fatty acid metabolism in cancer publication-title: Br. J. Cancer doi: 10.1038/s41416-019-0650-z – volume: 35 start-page: 123 year: 2013 ident: 10.1016/j.celrep.2021.109883_bib33 article-title: Multifaceted roles of PGE 2 in inflammation and cancer publication-title: Semin. Immunopathol. doi: 10.1007/s00281-012-0342-8 – volume: 43 start-page: 435 year: 2015 ident: 10.1016/j.celrep.2021.109883_bib5 article-title: Metabolic reprogramming of immune cells in cancer progression publication-title: Immunity doi: 10.1016/j.immuni.2015.09.001 – volume: 11 start-page: 736 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib56 article-title: Upregulation of CPT1A is essential for the tumor-promoting effect of adipocytes in colon cancer publication-title: Cell Death Dis. doi: 10.1038/s41419-020-02936-6 – volume: 22 start-page: 1289 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib22 article-title: Genetic manipulation of autonomic nerve fiber innervation and activity and its effect on breast cancer progression publication-title: Nat. Neurosci. doi: 10.1038/s41593-019-0430-3 – volume: 100 start-page: 463 year: 2016 ident: 10.1016/j.celrep.2021.109883_bib37 article-title: High-mobility group box protein 1 promotes the survival of myeloid-derived suppressor cells by inducing autophagy publication-title: J. Leukoc. Biol. doi: 10.1189/jlb.3HI0715-305R – volume: 135 start-page: 1425 year: 2015 ident: 10.1016/j.celrep.2021.109883_bib35 article-title: Kruppel-like factor KLF4 facilitates cutaneous wound healing by promoting fibrocyte generation from myeloid-derived suppressor cells publication-title: J. Invest. Dermatol. doi: 10.1038/jid.2015.3 – volume: 21 start-page: 485 year: 2021 ident: 10.1016/j.celrep.2021.109883_bib51 article-title: Myeloid-derived suppressor cells in the era of increasing myeloid cell diversity publication-title: Nat. Rev. Immunol. doi: 10.1038/s41577-020-00490-y – volume: 36 start-page: 81 year: 2015 ident: 10.1016/j.celrep.2021.109883_bib29 article-title: Fatty acid metabolism in the regulation of T cell function publication-title: Trends Immunol. doi: 10.1016/j.it.2014.12.005 – volume: 2019 start-page: 3809308 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib44 article-title: Recent insights into the mitochondrial role in autophagy and its regulation by oxidative stress publication-title: Oxid. Med. Cell. Longev. doi: 10.1155/2019/3809308 – volume: 362 start-page: 104297 year: 2021 ident: 10.1016/j.celrep.2021.109883_bib38 article-title: MDSCs, ageing and inflammageing publication-title: Cell. Immunol. doi: 10.1016/j.cellimm.2021.104297 – volume: 341 start-page: 1236361 year: 2013 ident: 10.1016/j.celrep.2021.109883_bib30 article-title: Autonomic nerve development contributes to prostate cancer progression publication-title: Science doi: 10.1126/science.1236361 – volume: 13 start-page: 18 year: 2012 ident: 10.1016/j.celrep.2021.109883_bib16 article-title: Immunosuppressive activity enhances central carbon metabolism and bioenergetics in myeloid-derived suppressor cells in vitro models publication-title: BMC Cell Biol. doi: 10.1186/1471-2121-13-18 – volume: 28 start-page: 87 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib28 article-title: Aerobic glycolysis controls myeloid-derived suppressor cells and tumor immunity via a specific CEBPB isoform in triple-negative breast cancer publication-title: Cell Metab. doi: 10.1016/j.cmet.2018.04.022 – volume: 110 start-page: 20176 year: 2013 ident: 10.1016/j.celrep.2021.109883_bib23 article-title: Baseline tumor growth and immune control in laboratory mice are significantly influenced by subthermoneutral housing temperature publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.1304291110 – volume: 68 start-page: 11 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib39 article-title: β-Adrenergic signaling blocks murine CD8+ T-cell metabolic reprogramming during activation: a mechanism for immunosuppression by adrenergic stress publication-title: Cancer Immunol. Immunother. doi: 10.1007/s00262-018-2243-8 – volume: 67 start-page: 4507 year: 2007 ident: 10.1016/j.celrep.2021.109883_bib46 article-title: Prostaglandin E2 promotes tumor progression by inducing myeloid-derived suppressor cells publication-title: Cancer Res. doi: 10.1158/0008-5472.CAN-06-4174 – volume: 14 start-page: 280 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib17 article-title: Neuronal autophagy aggravates microglial inflammatory injury by downregulating CX3CL1/fractalkine after ischemic stroke publication-title: Neural Regen. Res. doi: 10.4103/1673-5374.244793 – volume: 77 start-page: 5639 year: 2017 ident: 10.1016/j.celrep.2021.109883_bib8 article-title: β-adrenergic signaling in mice housed at standard temperatures suppresses an effector phenotype in CD8+ T cells and undermines checkpoint inhibitor therapy publication-title: Cancer Res. doi: 10.1158/0008-5472.CAN-17-0546 – volume: 122 start-page: 23 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib20 article-title: Energy metabolism manipulates the fate and function of tumour myeloid-derived suppressor cells publication-title: Br. J. Cancer doi: 10.1038/s41416-019-0644-x – volume: 10 start-page: 115 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib9 article-title: Differential regulation of human Treg and Th17 cells by fatty acid synthesis and glycolysis publication-title: Front. Immunol. doi: 10.3389/fimmu.2019.00115 – volume: 11 start-page: 4056 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib7 article-title: Autophagy regulates fatty acid availability for oxidative phosphorylation through mitochondria-endoplasmic reticulum contact sites publication-title: Nat. Commun. doi: 10.1038/s41467-020-17882-2 – volume: 4 start-page: 13 year: 2006 ident: 10.1016/j.celrep.2021.109883_bib48 article-title: Oxidative metabolism and PGC-1β attenuate macrophage-mediated inflammation publication-title: Cell Metab. doi: 10.1016/j.cmet.2006.05.011 – volume: 6 start-page: e1344804 year: 2017 ident: 10.1016/j.celrep.2021.109883_bib2 article-title: Exogenous lipid uptake induces metabolic and functional reprogramming of tumor-associated myeloid-derived suppressor cells publication-title: OncoImmunology doi: 10.1080/2162402X.2017.1344804 – volume: 120 start-page: 16 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib15 article-title: Immunosuppression mediated by myeloid-derived suppressor cells (MDSCs) during tumour progression publication-title: Br. J. Cancer doi: 10.1038/s41416-018-0333-1 – volume: 110 start-page: 15289 year: 2013 ident: 10.1016/j.celrep.2021.109883_bib52 article-title: Reprogramming of G protein-coupled receptor recycling and signaling by a kinase switch publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.1306340110 – volume: 34 start-page: 1 year: 2016 ident: 10.1016/j.celrep.2021.109883_bib21 article-title: Role of lipids in the metabolism and activation of immune cells publication-title: J. Nutr. Biochem. doi: 10.1016/j.jnutbio.2015.11.002 – volume: 33 start-page: 5967 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib32 article-title: CD11b+Ly6G+ myeloid-derived suppressor cells promote liver regeneration in a murine model of major hepatectomy publication-title: FASEB J. doi: 10.1096/fj.201801733R – volume: 11 start-page: 1371 year: 2020 ident: 10.1016/j.celrep.2021.109883_bib58 article-title: Myeloid-Derived Suppressor Cells in Tumors: From Mechanisms to Antigen Specificity and Microenvironmental Regulation publication-title: Front. Immunol. doi: 10.3389/fimmu.2020.01371 – volume: 27 start-page: 87 year: 2021 ident: 10.1016/j.celrep.2021.109883_bib13 article-title: Phase I Clinical Trial of Combination Propranolol and Pembrolizumab in Locally Advanced and Metastatic Melanoma: Safety, Tolerability, and Preliminary Evidence of Antitumor Activity publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-20-2381 – volume: 3 start-page: 47 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib55 article-title: Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma publication-title: Cell Stress doi: 10.15698/cst2019.02.176 – volume: 44 start-page: W90 issue: W1 year: 2016 ident: 10.1016/j.celrep.2021.109883_bib26 article-title: Enrichr: a comprehensive gene set enrichment analysis web server 2016 update publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkw377 – volume: 10 start-page: 172 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib54 article-title: MDSCs: Key Criminals of Tumor Pre-metastatic Niche Formation publication-title: Front. Immunol. doi: 10.3389/fimmu.2019.00172 – volume: 569 start-page: 73 year: 2019 ident: 10.1016/j.celrep.2021.109883_bib50 article-title: Fatty acid transport protein 2 reprograms neutrophils in cancer publication-title: Nature doi: 10.1038/s41586-019-1118-2 – volume: 283 start-page: 213 year: 2018 ident: 10.1016/j.celrep.2021.109883_bib43 article-title: Fatty acid metabolism in CD8+ T cell memory: challenging current concepts publication-title: Immunol. Rev. doi: 10.1111/imr.12655 – volume: 113 start-page: 523 year: 2007 ident: 10.1016/j.celrep.2021.109883_bib42 article-title: Adrenergic pharmacology and cognition: focus on the prefrontal cortex publication-title: Pharmacol. Ther. doi: 10.1016/j.pharmthera.2006.11.006
SSID	ssj0000601194
Score	2.5780172
Snippet	Myeloid-derived suppressor cells (MDSCs) impede antitumor immunity; however, the precise mechanisms that regulate their suppressive function remain unresolved....
SourceID	pubmedcentral proquest pubmed crossref elsevier
SourceType	Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	109883
SubjectTerms	Animals autophagy cancer fatty acid oxidation immune suppression Lipid Metabolism - genetics Lipid Metabolism - immunology MDSCs metabolism Mice Mice, Knockout Myeloid-Derived Suppressor Cells - metabolism Neoplasm Proteins - genetics Neoplasm Proteins - immunology Neoplasms - genetics Neoplasms - immunology Oxidative Phosphorylation prostaglandin E2 Receptors, Adrenergic, beta-2 - genetics Receptors, Adrenergic, beta-2 - immunology Signal Transduction - immunology stress Tumor Microenvironment - genetics Tumor Microenvironment - immunology β-adrenergic signaling
Title	β2-adrenergic receptor signaling regulates metabolic pathways critical to myeloid-derived suppressor cell function within the TME
URI	https://dx.doi.org/10.1016/j.celrep.2021.109883 https://www.ncbi.nlm.nih.gov/pubmed/34706232 https://www.proquest.com/docview/2587765556 https://pubmed.ncbi.nlm.nih.gov/PMC8601406
Volume	37
WOSCitedRecordID	wos000711887800003&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 2211-1247 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000601194 issn: 2211-1247 databaseCode: DOA dateStart: 20120101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3dbtMwFLa6ARI3iH_Kz2QkdhWlap04Ti5HVQTSOiFWpN5FTuKyTm1SJe1Yb3kk3oAX4Jk4J47TtBsaIHETRU4cO-d8sc85OT-EvBE8jqNuwOxEcdd2JQvsiAeODaslcyY89mWvDBQ-Ficn_ngcfGy1fphYmIuZSFP_8jJY_FdWQxswG0Nn_4Ld9UOhAc6B6XAEtsPxjxh_2B8cvgXdT2KMtsq_lDma0Xklyy301pBlAHqua9CrAmtIAxAw1zVWJ_4q14UVm_oHIJjO12qWTROgcg4LY2IVq0XpOwtPQ6O_hRtjiSG06FZOk6PhoCn09vE-83MC_xqbOLGGGWKYncn5XCYLeEW9Hc5r2A5lw4QNnVUOw33qbEyKfSCDRou2D1nH9cWjKK-sSadlFooPnaadg5WOdjqYXhvfTADOln8oY-iRx3TSzo66pq1a5HVmmQrM7rV7hzZjnHeAeECSDs4Bk235utDOTlbuUxwFBwGVGUuHjPfILSZ4EDS0ei0MYFI99G2op2UCOEsvw6uD_U5AuqoA7frxNgSj0X1yr9Jo6JFG4gPSUulDckfXOF0_It9-fm9ikRos0hqLtMYirbFIDRapwSJdZnQHi3SDRYpYpAaLVGORAhYpYPEx-fxuMOq_t6vCH3bses7S9rwJl92JK2MH9kBHsUi6nPMoBuU-gt2Z9SbMwT_USmE1AwZSrHAVJjcEcTzg0nlC9tMsVc8I7YEs4kfC9ROlXA-0adC3ZRR4CsT2qKtYmziG2mFcZcXH4iyz0Lg_noeaRyHyKNQ8ahO77rXQWWFuuF8YRoaVZKsl1hDAd0PP14bvISz8SEyZqmxVhIz7QnhAFq9Nnmoc1HNxXNEFvQbeTmwhpL4Bk8pvX0mnZ2Vyed9Dm4v3_J9n_ILc3Xy-L8n-Ml-pV-R2fLGcFvkB2RNj_6D8Rn4BB0T2vA
linkProvider	Directory of Open Access Journals
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=%CE%B22-adrenergic+receptor+signaling+regulates+metabolic+pathways+critical+to+myeloid-derived+suppressor+cell+function+within+the+TME&rft.jtitle=Cell+reports+%28Cambridge%29&rft.au=Mohammadpour%2C+Hemn&rft.au=MacDonald%2C+Cameron+R.&rft.au=McCarthy%2C+Philip+L.&rft.au=Abrams%2C+Scott+I.&rft.date=2021-10-26&rft.pub=Elsevier+Inc&rft.issn=2211-1247&rft.eissn=2211-1247&rft.volume=37&rft.issue=4&rft_id=info:doi/10.1016%2Fj.celrep.2021.109883&rft.externalDocID=S221112472101353X
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2211-1247&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2211-1247&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2211-1247&client=summon