| First Author | Mendiratta SK | Year | 1997 |
| Journal | Immunity | Volume | 6 |
| Issue | 4 | Pages | 469-77 |
| PubMed ID | 9133426 | Mgi Jnum | J:39748 |
| Mgi Id | MGI:87097 | Doi | 10.1016/s1074-7613(00)80290-3 |
| Citation | Mendiratta SK, et al. (1997) CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4. Immunity 6(4):469-477 |
| abstractText | 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. |
