We observed the emergence of a novel population of γδ T cells expressing NK1.1 Ag in the peritoneal cavity of mice infected with Salmonella choleraesuis. The NK1.1+γδ T cells accounted for approximately 20% of all γδ T cells emerging in the peritoneal cavity of C57BL/6 mice and expressed preferentially rearranged Vγ4-Jγ1 and Vδ6.3-Dδ1-Dδ2.Jδ1 genes with N diversity. The γδ T cells proliferated vigorously in response to PHA- treated spleen cells and produced IFN-γ, in the culture supernatant. However, spleen cells from Aβb-deficient mice were unable to stimulate the γδ T cells. Furthermore, the NK1.1+γδ T cells were stimulated not only by Chinese hamster ovary (CHO) cells expressing wild-type IA(b) but also by those expressing IA(b)/Eα52-68 or IA(b)/pigeon cytochrome c-derived analogue peptide complex. These proliferation activities were inhibited by mAb specific for IA(b) chain. Consistent with these findings, the emergence of NK1.1+ γδT cells was reduced in the peritoneal cavity of Aβ(b)-deficient mice after Salmonella infection, whereas NK1.1+ γδ T cells were rather abundant in the peritoneal cavity of Salmonella-infected β2m-deficient mice. Moreover, the NK1.1+ γδ T cells were easily identified in the thymus of β2m-deficient but not Aβb-deficient mice. Our results indicated that MHC class II expression is essential for development and activation of NK1.1+ γδ T cells in the thymus and the periphery.
|ジャーナル||Journal of Immunology|
|出版ステータス||出版済み - 2月 1 1999|
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