Tumor-associated macrophages promote intratumoral conversion of conventional CD4+ T cells into regulatory T cells via PD-1 signalling

While regulatory T cells (T regs ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophage...

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Vydáno v:	Oncoimmunology Ročník 11; číslo 1; s. 2063225
Hlavní autoři:	Kos, Kevin, Salvagno, Camilla, Wellenstein, Max D., Aslam, Muhammad A., Meijer, Denize A., Hau, Cheei-Sing, Vrijland, Kim, Kaldenbach, Daphne, Raeven, Elisabeth A.M., Schmittnaegel, Martina, Ries, Carola H., de Visser, Karin E.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Taylor & Francis 31.12.2022 Taylor & Francis Group
Témata:	Breast cancer immunology Breast Neoplasms Female Humans Immune Tolerance Original Research Programmed Cell Death 1 Receptor regulatory T cells T cell plasticity T-Lymphocytes, Regulatory Tumor Microenvironment Tumor-Associated Macrophages regulatory T cells Breast cancer immunology T cell plasticity tumor-associated macrophages
ISSN:	2162-402X, 2162-4011, 2162-402X
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Abstract	While regulatory T cells (T regs ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of T regs by promoting the conversion of conventional CD4 + T cells (T convs ) into T regs . Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4 + T convs into T regs in vitro, we additionally show that TAMs enhance PD-1 expression on CD4 + T cells. This indirectly contributes to the intratumoral accumulation of T regs , as loss of PD-1 on CD4 + T convs abrogates intratumoral conversion of adoptively transferred CD4 + T convs into T regs . Combined, this study provides insights into the complex immune cell crosstalk between CD4 + T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of T regs in breast tumors.
AbstractList	While regulatory T cells (T regs ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of T regs by promoting the conversion of conventional CD4 + T cells (T convs ) into T regs . Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4 + T convs into T regs in vitro, we additionally show that TAMs enhance PD-1 expression on CD4 + T cells. This indirectly contributes to the intratumoral accumulation of T regs , as loss of PD-1 on CD4 + T convs abrogates intratumoral conversion of adoptively transferred CD4 + T convs into T regs . Combined, this study provides insights into the complex immune cell crosstalk between CD4 + T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of T regs in breast tumors. While regulatory T cells (Tregs) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of Tregs by promoting the conversion of conventional CD4+ T cells (Tconvs) into Tregs. Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4+ Tconvs into Tregs in vitro, we additionally show that TAMs enhance PD-1 expression on CD4+ T cells. This indirectly contributes to the intratumoral accumulation of Tregs, as loss of PD-1 on CD4+ Tconvs abrogates intratumoral conversion of adoptively transferred CD4+ Tconvs into Tregs. Combined, this study provides insights into the complex immune cell crosstalk between CD4+ T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of Tregs in breast tumors. While regulatory T cells (Tregs) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of Tregs by promoting the conversion of conventional CD4+ T cells (Tconvs) into Tregs. Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4+ Tconvs into Tregs in vitro, we additionally show that TAMs enhance PD-1 expression on CD4+ T cells. This indirectly contributes to the intratumoral accumulation of Tregs, as loss of PD-1 on CD4+ Tconvs abrogates intratumoral conversion of adoptively transferred CD4+ Tconvs into Tregs. Combined, this study provides insights into the complex immune cell crosstalk between CD4+ T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of Tregs in breast tumors. While regulatory T cells (T ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of T by promoting the conversion of conventional CD4 T cells (T ) into T . Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4 T into T , we additionally show that TAMs enhance PD-1 expression on CD4 T cells. This indirectly contributes to the intratumoral accumulation of T , as loss of PD-1 on CD4 T abrogates intratumoral conversion of adoptively transferred CD4 T into T . Combined, this study provides insights into the complex immune cell crosstalk between CD4 T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of T in breast tumors. While regulatory T cells (Tregs) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of Tregs by promoting the conversion of conventional CD4+ T cells (Tconvs) into Tregs. Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4+ Tconvs into Tregsin vitro, we additionally show that TAMs enhance PD-1 expression on CD4+ T cells. This indirectly contributes to the intratumoral accumulation of Tregs, as loss of PD-1 on CD4+ Tconvs abrogates intratumoral conversion of adoptively transferred CD4+ Tconvs into Tregs. Combined, this study provides insights into the complex immune cell crosstalk between CD4+ T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of Tregs in breast tumors.While regulatory T cells (Tregs) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within tumors has been poorly characterized. Here, using spontaneous models for breast cancer, we demonstrate that tumor-associated macrophages (TAMs) contribute to the intratumoral accumulation of Tregs by promoting the conversion of conventional CD4+ T cells (Tconvs) into Tregs. Mechanistically, two processes were identified that independently contribute to this process. While TAM-derived TGF-β directly promotes the conversion of CD4+ Tconvs into Tregsin vitro, we additionally show that TAMs enhance PD-1 expression on CD4+ T cells. This indirectly contributes to the intratumoral accumulation of Tregs, as loss of PD-1 on CD4+ Tconvs abrogates intratumoral conversion of adoptively transferred CD4+ Tconvs into Tregs. Combined, this study provides insights into the complex immune cell crosstalk between CD4+ T cells and TAMs in the tumor microenvironment of breast cancer, and further highlights that therapeutic exploitation of macrophages may be an attractive immune intervention to limit the accumulation of Tregs in breast tumors.
Author	Schmittnaegel, Martina Salvagno, Camilla Vrijland, Kim Hau, Cheei-Sing Kaldenbach, Daphne Ries, Carola H. Meijer, Denize A. Kos, Kevin Aslam, Muhammad A. Wellenstein, Max D. Raeven, Elisabeth A.M. de Visser, Karin E.
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/35481289$$D View this record in MEDLINE/PubMed
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Cites_doi	10.1126/scitranslmed.3003130 10.1038/S41587-020-0546-8 10.1158/1078-0432.CCR-16-2569 10.1186/s12885-018-4441-3 10.1002/eji.201344423 10.1073/pnas.1812266115 10.1038/icb.2016.34 10.3389/FONC.2021.693517 10.1186/s40425-019-0701-2 10.1038/s41586-021-03651-8 10.1038/s41586-019-1450-6 10.1073/pnas.0506580102 10.1002/eji.200939432 10.1038/nature10772 10.1016/j.immuni.2016.10.032 10.1073/pnas.1316796110 10.1084/jem.20090847 10.1016/J.CCR.2014.05.016/ATTACHMENT/F3D8FA6C-225D-4C36-AFE0-D118A8052AB2/MMC1.PDF 10.1073/pnas.2004810117 10.1038/mi.2010.7 10.1016/j.celrep.2022.110447 10.1084/jem.20130762 10.1038/s41590-019-0429-7 10.1002/cyto.a.22451 10.1002/IJC.23392 10.1016/bs.mie.2019.07.035 10.3389/FIMMU.2018.02594 10.1038/s41467-020-17750-z 10.1073/pnas.1822001116 10.3390/cancers12113401 10.1146/annurev.immunol.25.022106.141623 10.1016/j.celrep.2019.09.067 10.1038/nprot.2017.083 10.1038/s41591-019-0357-y 10.1038/s41591-018-0014-x 10.1615/critrevimmunol.v30.i5.30 10.1182/blood-2011-09-379214 10.1080/2162402X.2018.1448329 10.1016/j.intimp.2019.106113 10.1158/0008-5472.CAN-08-4619 10.1016/j.ctrv.2018.08.010 10.1016/j.cels.2015.12.004 10.1038/s41556-019-0298-1 10.1038/cr.2017.34 10.1038/emm.2017.313 10.1038/nature08750 10.1158/2159-8290.CD-16-0577 10.1038/s41577-019-0271-z 10.4049/jimmunol.1500146 10.1371/JOURNAL.PPAT.1005270 10.1111/imm.12671 10.1146/annurev-cancerbio-042920-104912 10.1016/j.ccr.2006.09.013 10.1186/s12885-015-1742-7 10.1016/j.immuni.2018.05.006 10.1038/s41577-019-0127-6 10.1038/s41590-020-0769-3 10.1158/0008-5472.CAN-16-0984 10.1093/nar/gku936 10.1200/JCO.2006.05.9584 10.1158/0008-5472.CAN-11-4208 10.1126/scitranslmed.abd1616 10.1016/j.it.2016.08.012 10.1016/j.immuni.2018.04.013
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Keywords	regulatory T cells Breast cancer immunology T cell plasticity tumor-associated macrophages
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References_xml	– ident: e_1_3_6_19_1 doi: 10.1126/scitranslmed.3003130 – ident: e_1_3_6_32_1 doi: 10.1038/S41587-020-0546-8 – ident: e_1_3_6_4_1 doi: 10.1158/1078-0432.CCR-16-2569 – ident: e_1_3_6_5_1 doi: 10.1186/s12885-018-4441-3 – ident: e_1_3_6_59_1 doi: 10.1002/eji.201344423 – ident: e_1_3_6_25_1 doi: 10.1073/pnas.1812266115 – ident: e_1_3_6_27_1 doi: 10.1038/icb.2016.34 – ident: e_1_3_6_54_1 doi: 10.3389/FONC.2021.693517 – ident: e_1_3_6_39_1 doi: 10.1186/s40425-019-0701-2 – ident: e_1_3_6_26_1 doi: 10.1038/s41586-021-03651-8 – ident: e_1_3_6_30_1 doi: 10.1038/s41586-019-1450-6 – ident: e_1_3_6_63_1 doi: 10.1073/pnas.0506580102 – ident: e_1_3_6_51_1 doi: 10.1002/eji.200939432 – ident: e_1_3_6_17_1 doi: 10.1038/nature10772 – ident: e_1_3_6_23_1 doi: 10.1016/j.immuni.2016.10.032 – ident: e_1_3_6_24_1 doi: 10.1073/pnas.1316796110 – ident: e_1_3_6_43_1 doi: 10.1084/jem.20090847 – ident: e_1_3_6_33_1 doi: 10.1016/J.CCR.2014.05.016/ATTACHMENT/F3D8FA6C-225D-4C36-AFE0-D118A8052AB2/MMC1.PDF – ident: e_1_3_6_65_1 doi: 10.1073/pnas.2004810117 – ident: e_1_3_6_14_1 doi: 10.1038/mi.2010.7 – ident: e_1_3_6_9_1 doi: 10.1016/j.celrep.2022.110447 – ident: e_1_3_6_8_1 doi: 10.1084/jem.20130762 – ident: e_1_3_6_40_1 doi: 10.1038/s41590-019-0429-7 – ident: e_1_3_6_62_1 doi: 10.1002/cyto.a.22451 – ident: e_1_3_6_35_1 doi: 10.1002/IJC.23392 – ident: e_1_3_6_61_1 doi: 10.1016/bs.mie.2019.07.035 – ident: e_1_3_6_36_1 doi: 10.3389/FIMMU.2018.02594 – ident: e_1_3_6_55_1 doi: 10.1038/s41467-020-17750-z – ident: e_1_3_6_45_1 doi: 10.1073/pnas.1822001116 – ident: e_1_3_6_56_1 doi: 10.3390/cancers12113401 – ident: e_1_3_6_13_1 doi: 10.1146/annurev.immunol.25.022106.141623 – ident: e_1_3_6_41_1 doi: 10.1016/j.celrep.2019.09.067 – ident: e_1_3_6_48_1 doi: 10.1038/nprot.2017.083 – ident: e_1_3_6_44_1 doi: 10.1038/s41591-019-0357-y – ident: e_1_3_6_2_1 doi: 10.1038/s41591-018-0014-x – ident: e_1_3_6_38_1 doi: 10.1615/critrevimmunol.v30.i5.30 – ident: e_1_3_6_34_1 doi: 10.1182/blood-2011-09-379214 – ident: e_1_3_6_60_1 doi: 10.1080/2162402X.2018.1448329 – ident: e_1_3_6_21_1 doi: 10.1016/j.intimp.2019.106113 – ident: e_1_3_6_22_1 doi: 10.1158/0008-5472.CAN-08-4619 – ident: e_1_3_6_28_1 doi: 10.1016/j.ctrv.2018.08.010 – ident: e_1_3_6_42_1 doi: 10.1016/j.cels.2015.12.004 – ident: e_1_3_6_31_1 doi: 10.1038/s41556-019-0298-1 – ident: e_1_3_6_52_1 doi: 10.1038/cr.2017.34 – ident: e_1_3_6_12_1 doi: 10.1038/emm.2017.313 – ident: e_1_3_6_15_1 doi: 10.1038/nature08750 – ident: e_1_3_6_11_1 doi: 10.1158/2159-8290.CD-16-0577 – ident: e_1_3_6_3_1 doi: 10.1038/s41577-019-0271-z – ident: e_1_3_6_57_1 doi: 10.4049/jimmunol.1500146 – ident: e_1_3_6_47_1 doi: 10.1371/JOURNAL.PPAT.1005270 – ident: e_1_3_6_50_1 doi: 10.1111/imm.12671 – ident: e_1_3_6_10_1 doi: 10.1146/annurev-cancerbio-042920-104912 – ident: e_1_3_6_29_1 doi: 10.1016/j.ccr.2006.09.013 – ident: e_1_3_6_7_1 doi: 10.1186/s12885-015-1742-7 – ident: e_1_3_6_20_1 doi: 10.1016/j.immuni.2018.05.006 – ident: e_1_3_6_53_1 doi: 10.1038/s41577-019-0127-6 – ident: e_1_3_6_46_1 doi: 10.1038/s41590-020-0769-3 – ident: e_1_3_6_37_1 doi: 10.1158/0008-5472.CAN-16-0984 – ident: e_1_3_6_49_1 doi: 10.1093/nar/gku936 – ident: e_1_3_6_6_1 doi: 10.1200/JCO.2006.05.9584 – ident: e_1_3_6_64_1 doi: 10.1158/0008-5472.CAN-11-4208 – ident: e_1_3_6_58_1 doi: 10.1126/scitranslmed.abd1616 – ident: e_1_3_6_18_1 doi: 10.1016/j.it.2016.08.012 – ident: e_1_3_6_16_1 doi: 10.1016/j.immuni.2018.04.013
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Snippet	While regulatory T cells (T regs ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk... While regulatory T cells (T ) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk within... While regulatory T cells (Tregs) and macrophages have been recognized as key orchestrators of cancer-associated immunosuppression, their cellular crosstalk...
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SubjectTerms	Breast cancer immunology Breast Neoplasms Female Humans Immune Tolerance Original Research Programmed Cell Death 1 Receptor regulatory T cells T cell plasticity T-Lymphocytes, Regulatory Tumor Microenvironment Tumor-Associated Macrophages
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Title	Tumor-associated macrophages promote intratumoral conversion of conventional CD4+ T cells into regulatory T cells via PD-1 signalling
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