FOXP3型
免疫抑制
癌症研究
肿瘤微环境
三阴性乳腺癌
乳腺癌
生物
白细胞介素2受体
效应器
免疫学
T细胞
免疫系统
化学
癌症
遗传学
作者
Ana Costa,Yann Kieffer,Alix Scholer‐Dahirel,Floriane Pelon,Brigitte Bourachot,Mélissa Cardon,Philémon Sirven,Ilaria Magagna,Laetitia Fuhrmann,Charles Bernard,Claire Bonneau,Maria Kondratova,Inna Kuperstein,Andreï Zinovyev,Anne-Marie Givel,Maria‐Carla Parrini,Vassili Soumelis,Anne Vincent‐Salomon,Fatima Mechta‐Grigoriou
出处
期刊:Cancer Cell
[Elsevier]
日期:2018-02-15
卷期号:33 (3): 463-479.e10
被引量:1240
标识
DOI:10.1016/j.ccell.2018.01.011
摘要
Carcinoma-associated fibroblasts (CAF) are key players in the tumor microenvironment. Here, we characterize four CAF subsets in breast cancer with distinct properties and levels of activation. Two myofibroblastic subsets (CAF-S1, CAF-S4) accumulate differentially in triple-negative breast cancers (TNBC). CAF-S1 fibroblasts promote an immunosuppressive environment through a multi-step mechanism. By secreting CXCL12, CAF-S1 attracts CD4+CD25+ T lymphocytes and retains them by OX40L, PD-L2, and JAM2. Moreover, CAF-S1 increases T lymphocyte survival and promotes their differentiation into CD25HighFOXP3High, through B7H3, CD73, and DPP4. Finally, in contrast to CAF-S4, CAF-S1 enhances the regulatory T cell capacity to inhibit T effector proliferation. These data are consistent with FOXP3+ T lymphocyte accumulation in CAF-S1-enriched TNBC and show how a CAF subset contributes to immunosuppression.
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