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首页> 外文期刊>Cancer Cell >CXCR2-Expressing Myeloid-Derived Suppressor Cells Are Essential to Promote Colitis-Associated Tumorigenesis
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CXCR2-Expressing Myeloid-Derived Suppressor Cells Are Essential to Promote Colitis-Associated Tumorigenesis

机译：表达CXCR2的髓样抑制细胞对于促进结肠炎相关的肿瘤发生至关重要。

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摘要

A large body of evidence indicates that chronic inflammation is one of several key risk factors for cancer initiation, progression, and metastasis. However, the underlying mechanisms responsible for the contribution of inflammation and inflammatory mediators to cancer remain elusive. Here, we present genetic evidence that loss of CXCR2 dramatically suppresses chronic colonic inflammation and colitis-associated tumorigenesis through inhibiting infiltration of myeloid-derived suppressor cells (MDSCs) into colonic mucosa and tumors in a mouse model of colitis-associated cancer. CXCR2 ligands were elevated in inflamed colonic mucosa and tumors and induced MDSC chemotaxis. Adoptive transfer of wild-type MDSCs into Cxcr2-/- mice restored AOM/DSS-induced tumor progression. MDSCs accelerated tumor growth by inhibiting CD8+ Tcell cytotoxic activity.
机译：大量证据表明，慢性炎症是癌症发生，进展和转移的几个关键风险因素之一。然而，引起炎症和炎症介质对癌症的贡献的潜在机制仍然难以捉摸。在这里，我们提供了遗传证据，证明了CXCR2的丧失通过抑制骨髓来源的抑制细胞（MDSCs）浸入结肠粘膜相关癌的小鼠模型中的结肠黏膜和肿瘤中，从而显着抑制了慢性结肠炎和结肠炎相关的肿瘤发生。 CXCR2配体在发炎的结肠粘膜和肿瘤中升高，并诱导MDSC趋化性。野生型MDSCs过继转移到Cxcr2-/-小鼠中恢复了AOM / DSS诱导的肿瘤进展。 MDSC通过抑制CD8 + T细胞的细胞毒活性来促进肿瘤的生长。

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