CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4

被引:540
作者
Mendiratta, SK [1 ]
Martin, WD [1 ]
Hong, S [1 ]
Boesteanu, A [1 ]
Joyce, S [1 ]
VanKaer, L [1 ]
机构
[1] PENN STATE UNIV,COLL MED,DEPT MICROBIOL & IMMUNOL,MILTON S HERSHEY MED CTR,HERSHEY,PA 17003
关键词
D O I
10.1016/S1074-7613(00)80290-3
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
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收藏
页码:469 / 477
页数:9
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