Impaired NK1(+) T cell development and early IL-4 production in CD1-deficient mice
Impaired NK1(+) T cell development and early IL-4 production in CD1-deficient mice
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DOI：
10.1016/s1074-7613(00)80289-7
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发表时间：
1997-04-01
期刊：
影响因子：
32.4
通讯作者：
Wang, CR
中科院分区：
文献类型：
--
作者：
Chen, YH;Chiu, NM;Wang, CR
MHC Ib 类分子 CD1 在整个哺乳动物进化过程中一直保守。为了评估 CD1 在淋巴细胞发育中的功能，我们培育了靶向破坏 CD1.1 和 CD1.2 基因的小鼠。 CD1缺陷小鼠的CD4(+)和CD8(+) T细胞数量正常，但携带NK1.1的T细胞显着减少，特别是那些具有V alpha 14-J alpha 281经典基因重排的T细胞。CD1缺陷小鼠在全身T细胞激活后无法产生快速的IL-4反应，但可以产生有效的抗原特异性Th2反应。因此，CD1对于具有单形抗原受体的特化T淋巴细胞亚群的发育是必需的。这些 T 细胞的快速效应细胞因子分泌表明 CD1 可以教育适应性免疫细胞以促进先天免疫功能。
The MHC class Ib molecule, CD1, has been conserved throughout mammalian evolution. To assess the function of CD1 in lymphocyte development, we generated mice with targeted disruption of the CD1.1 and CD1.2 genes. CD1-deficient mice have normal numbers of CD4(+) and CD8(+) T cells but marked reduction in NK1.1-bearing T cells, particularly those with a canonical gene rearrangement of V alpha 14-J alpha 281. CD1-deficient mice are unable to generate a rapid IL-4 response following systemic T cell activation but can generate effective antigen-specific Th2 responses. Thus, CD1 is required for the development of a specialized subset of T lymphocytes with a monomorphic antigen receptor. The rapid effector cytokine secretion of these T cells suggests that CD1 educates adaptive immune cells to subserve functions of innate immunity.