CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4
CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4
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DOI：
10.1016/s1074-7613(00)80290-3
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发表时间：
1997-04-01
期刊：
影响因子：
32.4
通讯作者：
VanKaer, L
中科院分区：
文献类型：
--
作者：
Mendiratta, SK;Martin, WD;VanKaer, L
小鼠CD1与一种被称为自然T（NT）细胞的特殊T细胞亚群的发育和功能有关，这种细胞共同表达T细胞受体（TCR）和自然杀伤细胞受体NK1.1。活化的NT细胞会迅速产生大量白细胞介素 - 4（IL - 4），这表明这些细胞能够影响CD4⁺效应T细胞亚群的分化。我们培育出了携带突变型CD1d1基因的小鼠。这些小鼠的胸腺、脾脏和肝脏中的NT细胞数量显著减少。来自突变小鼠的活化脾细胞不产生IL - 4，而经过类似处理的野生型脾细胞则分泌大量这种细胞因子。这些结果表明CD1在NT细胞的阳性选择和功能中起着关键作用。
Murine CD1 has been implicated in the development end function of an unusual subset of T cells, termed natural T (NT) cells, that coexpress the T cell receptor (TCR) and the natural killer cell receptor NK1.1. Activated NT cells promptly produce large amounts of IL-4, suggesting that these cells can influence the differentiation of CD4(+) effector T cell subsets. We have generated mice that carry a mutant CD1d1 gene. NT cell numbers in the thymus, spleen, and liver of these mice were dramatically reduced. Activated splenocytes from mutant mice did not produce IL-4, whereas similarly treated wild-type splenocytes secreted large amounts of this cytokine. These results demonstrate a critical role for CD1 in the positive selection and function of NT cells.