KLRG1 negatively regulates natural killer cell functions through the Akt pathway in individuals with chronic hepatitis C virus infection
In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients w...
Uloženo v:
| Vydáno v: | Journal of virology Ročník 87; číslo 21; s. 11626 |
|---|---|
| Hlavní autoři: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
01.11.2013
|
| Témata: | |
| ISSN: | 1098-5514, 1098-5514 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection. |
|---|---|
| AbstractList | In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection. In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection.In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56(+) NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1(+) NK cells, including CD56(bright) and CD56(dim) subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1(-) NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection. |
| Author | Wang, Jia M Moorman, Jonathan P Shi, Lei Yao, Zhi Q Ying, Ruo S Cheng, Yong Q Wu, Xiao Y Li, Guang Y |
| Author_xml | – sequence: 1 givenname: Jia M surname: Wang fullname: Wang, Jia M organization: Department of Internal Medicine, Division of Infectious Diseases, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA – sequence: 2 givenname: Yong Q surname: Cheng fullname: Cheng, Yong Q – sequence: 3 givenname: Lei surname: Shi fullname: Shi, Lei – sequence: 4 givenname: Ruo S surname: Ying fullname: Ying, Ruo S – sequence: 5 givenname: Xiao Y surname: Wu fullname: Wu, Xiao Y – sequence: 6 givenname: Guang Y surname: Li fullname: Li, Guang Y – sequence: 7 givenname: Jonathan P surname: Moorman fullname: Moorman, Jonathan P – sequence: 8 givenname: Zhi Q surname: Yao fullname: Yao, Zhi Q |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23966413$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNkF9LwzAUxYNM3B9981ny6Etn0iZZ-ziGzulAEPW1pOntGtels0k29g382EadIOfCuQ8_DpwzRD3TGkDokpIxpXF68_C2GBPKKY9ocoIGlGRpxDllvX9_Hw2tfSeEMibYGerHSSYEo8kAfT4un-cUG1hJp3fQHHAHK99IBxYb6XwnG7zWTQMdVtA0uPJGOd0ai13dtX5VBwc8XTu8la7eywPWJlypd7r0srF4r12NVWCNVriGQGmnLZ7hne68DWgFP4Hn6LQKPFwcfYRe725fZvfR8mm-mE2XkWKMu0gVVKkynQhZElkpXsaikCkXqUiplGyiZKwmmQJglDKRyjQWiSK8DEqAFmU8Qte_uduu_fBgXb7R9ruaNNB6m4eJEkZ4RkRAr46oLzZQ5ttOb2R3yP_Wi78Az0h1vA |
| CitedBy_id | crossref_primary_10_3390_cancers13235967 crossref_primary_10_1007_s00204_016_1809_5 crossref_primary_10_1007_s00262_020_02522_x crossref_primary_10_3390_ijms242115653 crossref_primary_10_1007_s13402_020_00523_7 crossref_primary_10_1016_j_lfs_2023_121997 crossref_primary_10_1016_j_fsi_2021_03_016 crossref_primary_10_3389_fimmu_2022_894508 crossref_primary_10_1073_pnas_2018834118 crossref_primary_10_1093_sleep_zsae160 crossref_primary_10_1016_j_tube_2022_102221 crossref_primary_10_3389_fimmu_2018_03001 crossref_primary_10_1038_s41467_024_46778_8 crossref_primary_10_1111_imm_12349 crossref_primary_10_1111_liv_14172 crossref_primary_10_3748_wjg_v21_i41_11522 crossref_primary_10_1038_s41591_023_02277_9 crossref_primary_10_4049_jimmunol_2300672 crossref_primary_10_1016_j_medj_2023_05_003 crossref_primary_10_1016_j_trim_2024_102068 crossref_primary_10_1111_1348_0421_12858 crossref_primary_10_1111_imm_12463 crossref_primary_10_1016_j_hlc_2019_10_018 crossref_primary_10_1016_j_lfs_2024_123301 crossref_primary_10_1515_sjecr_2016_0011 crossref_primary_10_3748_wjg_v22_i4_1449 crossref_primary_10_3389_fimmu_2022_1065570 crossref_primary_10_3390_cancers14194915 crossref_primary_10_1002_cyto_a_24941 crossref_primary_10_1017_S0031182022000828 crossref_primary_10_1093_infdis_jiy046 crossref_primary_10_1002_pro6_1165 crossref_primary_10_1111_liv_15054 crossref_primary_10_4049_jimmunol_1600590 crossref_primary_10_1007_s11684_018_0621_4 crossref_primary_10_1111_imcb_12739 crossref_primary_10_1016_j_bbi_2021_04_018 crossref_primary_10_1016_j_omto_2021_11_016 crossref_primary_10_1089_cbr_2018_2628 crossref_primary_10_1186_s12964_024_01714_7 crossref_primary_10_3390_biomedicines12030650 crossref_primary_10_5604_16652681_1184193 crossref_primary_10_3390_cells14110846 |
| ContentType | Journal Article |
| DBID | CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1128/JVI.01515-13 |
| DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic |
| 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 | no_fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1098-5514 |
| ExternalDocumentID | 23966413 |
| Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: NIDDK NIH HHS grantid: R01 DK093526 – fundername: NIAID NIH HHS grantid: 1R15AI103828-01 – fundername: NIAID NIH HHS grantid: R15 AI103828 – fundername: NIDDK NIH HHS grantid: R01DK093526 |
| GroupedDBID | --- -~X .55 .GJ 0R~ 18M 29L 2WC 39C 3O- 4.4 41~ 53G 5GY 5RE 5VS 6TJ 85S AAYJJ ABPPZ ACGFO ACNCT ADBBV AENEX AFFNX AGVNZ AI. ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BTFSW C1A CGR CS3 CUY CVF D0S DIK E3Z EBS ECM EIF EJD F5P FRP GX1 H13 HYE HZ~ IH2 KQ8 MVM N9A NPM O9- OHT OK1 P2P RHI RNS RPM RSF TR2 UPT VH1 W2D W8F WH7 WOQ X7M Y6R YQT ZGI ZXP ~02 ~KM 7X8 AAFWJ AAGFI AFPKN |
| ID | FETCH-LOGICAL-c445t-cb1ccd876ad0afc5d26ba8568681aa47ca2c79cee411468a8263c05d5d53e1bd2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 51 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000325863400027&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1098-5514 |
| IngestDate | Sun Nov 09 11:26:47 EST 2025 Thu Apr 03 07:08:17 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 21 |
| Language | English |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c445t-cb1ccd876ad0afc5d26ba8568681aa47ca2c79cee411468a8263c05d5d53e1bd2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://jvi.asm.org/content/jvi/87/21/11626.full.pdf |
| PMID | 23966413 |
| PQID | 1443405906 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_1443405906 pubmed_primary_23966413 |
| PublicationCentury | 2000 |
| PublicationDate | 2013-11-01 |
| PublicationDateYYYYMMDD | 2013-11-01 |
| PublicationDate_xml | – month: 11 year: 2013 text: 2013-11-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Journal of virology |
| PublicationTitleAlternate | J Virol |
| PublicationYear | 2013 |
| References | 12217400 - Mol Immunol. 2002 Sep;38(16-18):1307-13 11340207 - Science. 2001 May 4;292(5518):934-7 12915213 - Exp Gerontol. 2003 Aug;38(8):911-20 20034045 - Hepatology. 2010 Jan;51(1):8-11 21263070 - J Immunol. 2011 Mar 1;186(5):3093-103 1279801 - Science. 1992 Oct 2;258(5079):135-40 11698225 - Trends Immunol. 2001 Nov;22(11):633-40 16160163 - J Virol. 2005 Oct;79(19):12365-74 12133970 - J Immunol. 2002 Aug 1;169(3):1444-52 15218054 - J Leukoc Biol. 2004 Oct;76(4):743-59 23388728 - J Virol. 2013 Apr;87(8):4372-83 18424713 - J Immunol. 2008 May 1;180(9):5935-45 11673487 - J Immunol. 2001 Nov 1;167(9):4838-43 17553896 - J Virol. 2007 Sep;81(17):9292-8 16461340 - J Exp Med. 2006 Feb 20;203(2):289-95 15879103 - J Immunol. 2005 May 15;174(10):6088-94 20138830 - Biochem Biophys Res Commun. 2010 Mar 5;393(2):331-7 18759921 - Immunol Rev. 2008 Aug;224:70-84 17079288 - J Virol. 2007 Jan;81(2):945-53 15368283 - Eur J Immunol. 2004 Oct;34(10):2672-80 11884419 - J Immunol. 2002 Mar 15;168(6):2585-9 21637332 - PLoS One. 2011;6(5):e19664 15297676 - Science. 2004 Aug 6;305(5685):872-4 17307799 - Int Immunol. 2007 Apr;19(4):391-400 19406987 - Blood. 2009 Jun 25;113(26):6619-28 16424155 - J Immunol. 2006 Feb 1;176(3):1311-5 11244035 - Annu Rev Immunol. 2001;19:197-223 19552960 - Mol Immunol. 2009 Aug;46(13):2723-7 9842918 - Eur J Immunol. 1998 Nov;28(11):3755-62 12393723 - Blood. 2002 Nov 15;100(10):3698-702 16498647 - Liver Transpl. 2006 Mar;12(3):363-72 16322112 - Gut. 2006 Jun;55(6):869-77 20548953 - PLoS Pathog. 2010;6(6):e1000947 21040831 - Adv Virus Res. 2010;78:43-86 16140789 - J Virol. 2005 Sep;79(18):12112-6 10681285 - Ann Intern Med. 2000 Feb 15;132(4):296-305 20077564 - Hepatology. 2010 Apr;51(4):1168-75 20456039 - Liver Int. 2010 Apr;30(4):567-73 15210783 - J Immunol. 2004 Jul 1;173(1):259-66 15771571 - Annu Rev Immunol. 2005;23:225-74 15905121 - Hepatol Res. 2005 Aug;32(4):213-7 20597961 - Eur J Clin Invest. 2010 Sep;40(9):851-63 15185313 - Hepatology. 2004 Jun;39(6):1709-20 16122679 - Lancet Infect Dis. 2005 Sep;5(9):558-67 22378844 - Blood. 2012 Apr 12;119(15):3478-85 17931181 - Hepatol Res. 2007 Oct;37 Suppl 3:S319-26 22706088 - J Immunol. 2012 Jul 15;189(2):755-66 20812318 - Hepatology. 2010 Nov;52(5):1581-9 20334827 - Gastroenterology. 2010 May;138(5):1885-97 |
| References_xml | – reference: 22378844 - Blood. 2012 Apr 12;119(15):3478-85 – reference: 16461340 - J Exp Med. 2006 Feb 20;203(2):289-95 – reference: 12133970 - J Immunol. 2002 Aug 1;169(3):1444-52 – reference: 18424713 - J Immunol. 2008 May 1;180(9):5935-45 – reference: 20597961 - Eur J Clin Invest. 2010 Sep;40(9):851-63 – reference: 20138830 - Biochem Biophys Res Commun. 2010 Mar 5;393(2):331-7 – reference: 15905121 - Hepatol Res. 2005 Aug;32(4):213-7 – reference: 12217400 - Mol Immunol. 2002 Sep;38(16-18):1307-13 – reference: 20812318 - Hepatology. 2010 Nov;52(5):1581-9 – reference: 16140789 - J Virol. 2005 Sep;79(18):12112-6 – reference: 21040831 - Adv Virus Res. 2010;78:43-86 – reference: 15368283 - Eur J Immunol. 2004 Oct;34(10):2672-80 – reference: 20034045 - Hepatology. 2010 Jan;51(1):8-11 – reference: 20456039 - Liver Int. 2010 Apr;30(4):567-73 – reference: 15879103 - J Immunol. 2005 May 15;174(10):6088-94 – reference: 20077564 - Hepatology. 2010 Apr;51(4):1168-75 – reference: 9842918 - Eur J Immunol. 1998 Nov;28(11):3755-62 – reference: 10681285 - Ann Intern Med. 2000 Feb 15;132(4):296-305 – reference: 11244035 - Annu Rev Immunol. 2001;19:197-223 – reference: 11884419 - J Immunol. 2002 Mar 15;168(6):2585-9 – reference: 20548953 - PLoS Pathog. 2010;6(6):e1000947 – reference: 20334827 - Gastroenterology. 2010 May;138(5):1885-97 – reference: 16160163 - J Virol. 2005 Oct;79(19):12365-74 – reference: 17553896 - J Virol. 2007 Sep;81(17):9292-8 – reference: 17931181 - Hepatol Res. 2007 Oct;37 Suppl 3:S319-26 – reference: 21637332 - PLoS One. 2011;6(5):e19664 – reference: 16322112 - Gut. 2006 Jun;55(6):869-77 – reference: 12915213 - Exp Gerontol. 2003 Aug;38(8):911-20 – reference: 11673487 - J Immunol. 2001 Nov 1;167(9):4838-43 – reference: 21263070 - J Immunol. 2011 Mar 1;186(5):3093-103 – reference: 16122679 - Lancet Infect Dis. 2005 Sep;5(9):558-67 – reference: 19552960 - Mol Immunol. 2009 Aug;46(13):2723-7 – reference: 19406987 - Blood. 2009 Jun 25;113(26):6619-28 – reference: 18759921 - Immunol Rev. 2008 Aug;224:70-84 – reference: 17307799 - Int Immunol. 2007 Apr;19(4):391-400 – reference: 17079288 - J Virol. 2007 Jan;81(2):945-53 – reference: 16498647 - Liver Transpl. 2006 Mar;12(3):363-72 – reference: 11340207 - Science. 2001 May 4;292(5518):934-7 – reference: 15185313 - Hepatology. 2004 Jun;39(6):1709-20 – reference: 15297676 - Science. 2004 Aug 6;305(5685):872-4 – reference: 16424155 - J Immunol. 2006 Feb 1;176(3):1311-5 – reference: 11698225 - Trends Immunol. 2001 Nov;22(11):633-40 – reference: 15210783 - J Immunol. 2004 Jul 1;173(1):259-66 – reference: 22706088 - J Immunol. 2012 Jul 15;189(2):755-66 – reference: 15218054 - J Leukoc Biol. 2004 Oct;76(4):743-59 – reference: 12393723 - Blood. 2002 Nov 15;100(10):3698-702 – reference: 23388728 - J Virol. 2013 Apr;87(8):4372-83 – reference: 1279801 - Science. 1992 Oct 2;258(5079):135-40 – reference: 15771571 - Annu Rev Immunol. 2005;23:225-74 |
| SSID | ssj0014464 |
| Score | 2.3536441 |
| Snippet | In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells,... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 11626 |
| SubjectTerms | Apoptosis CD56 Antigen - analysis Cell Proliferation Female Hepatitis C, Chronic - immunology Humans Interferon-gamma - secretion Killer Cells, Natural - chemistry Killer Cells, Natural - immunology Lectins, C-Type - metabolism Male Signal Transduction Trans-Activators - metabolism |
| Title | KLRG1 negatively regulates natural killer cell functions through the Akt pathway in individuals with chronic hepatitis C virus infection |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/23966413 https://www.proquest.com/docview/1443405906 |
| Volume | 87 |
| WOSCitedRecordID | wos000325863400027&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LS-RAEG5c3QUvPtb1rZSw19Z0p_M6iYjjexhklbkNne6ODkpGJ6My_8CfbVUnoydhQQJJLg1JdVFVXVVffYz9jaSLY5taLoyMuHJJyPMkyDnGCloIHWWxR_HfXCTtdtrtZp0m4VY1bZUTm-gNtR0YypHvYeAfKkJKxvuPT5xYo6i62lBo_GAzIYYy1NKVdD-rCHjU8VVlmplJkcGk8V2me2c3p7sBOXNOxAZfBZfeybTmv_t5C2yuCS_hoNaHRTblyt_sV004OV5ib-cXV8cCSnfr530_jGFYc9G7CvyIT1x779GBQBl9IK_nFRMaPh98Oji4HwExGb_qMfRL6H9guiqgtC6YeuAu3Dlq1x71KziEl_7wuYJJ61f5h123jv4dnvCGi4EbpaIRN7kwxqLp1DbQhYmsjHOdRnEap0JrlRgtTZKhx1UEc041nlpCE0QWr9CJ3MplNl0OSrfKIBORTYOsKJwzyhiZ2bzQQuOrDpQRao3tTETcQ12n39WlGzxXvU8hr7GVep96j_VQjp4M8eCGHnn9P1ZvsFlJrBYeUrjJZgoUkNtiP80LimS47ZUI7-3O5Ts-pdTJ |
| linkProvider | ProQuest |
| 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=KLRG1+negatively+regulates+natural+killer+cell+functions+through+the+Akt+pathway+in+individuals+with+chronic+hepatitis+C+virus+infection&rft.jtitle=Journal+of+virology&rft.au=Wang%2C+Jia+M&rft.au=Cheng%2C+Yong+Q&rft.au=Shi%2C+Lei&rft.au=Ying%2C+Ruo+S&rft.date=2013-11-01&rft.issn=1098-5514&rft.eissn=1098-5514&rft.volume=87&rft.issue=21&rft.spage=11626&rft_id=info:doi/10.1128%2FJVI.01515-13&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1098-5514&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1098-5514&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1098-5514&client=summon |