在T细胞缺陷小鼠中揭示的Fas（CD95）的肿瘤抑制功能。
A tumor-suppressor function for Fas (CD95) revealed in T cell-deficient mice.
作者信息
Peng S L, Robert M E, Hayday A C, Craft J
机构信息
Section of Rheumatology, Yale University School of Medicine, New Haven, Connecticut, USA.
出版信息
J Exp Med. 1996 Sep 1;184(3):1149-54. doi: 10.1084/jem.184.3.1149.
Fas (CD95) and its ligand are central regulatory molecules in hematopoietic cells. Previous studies have suggested a role for Fas in the regulation of tumor progression, but Fas has not yet been conclusively identified as a tumor suppressor. Fas-deficient individuals lack malignant tumors, perhaps because of regulation by T cells. To investigate such a possibility, mice deficient in both T cells and Fas were generated, and they were found to develop severe B cell dysregulation characterized by malignant, lethal B cell lymphoma. Lymphoma arose from a monoclonal B220+CD19-CD5-CD23- B cell secreting immunoglobulin M, kappa rheumatoid factor. In contrast, animals containing alpha beta T cells, gamma delta T cells, and/or functional Fas suppressed the development of lymphoma. These data indicate that Fas functions as a tumor suppressor, and identifies roles for both alpha beta T cells and gamma delta T cells in Fas-independent tumor regulation.
Fas（CD95）及其配体是造血细胞中的核心调节分子。先前的研究表明Fas在肿瘤进展调节中发挥作用，但Fas尚未被确凿地鉴定为肿瘤抑制因子。Fas缺陷个体缺乏恶性肿瘤，这可能是由于T细胞的调节作用。为了研究这种可能性，构建了T细胞和Fas均缺陷的小鼠，发现它们出现了以恶性、致死性B细胞淋巴瘤为特征的严重B细胞失调。淋巴瘤起源于分泌免疫球蛋白M、κ类风湿因子的单克隆B220⁺CD19⁻CD5⁻CD23⁻B细胞。相比之下，含有αβT细胞、γδT细胞和/或功能性Fas的动物抑制了淋巴瘤的发展。这些数据表明Fas作为肿瘤抑制因子发挥作用，并确定了αβT细胞和γδT细胞在不依赖Fas的肿瘤调节中的作用。
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