MHC Class II-Dependent NK1.1+ γδ T Cells Are Induced in Mice bySalmonellaInfection

Abstract

AbstractWe 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 IAb but also by those expressing IAb/Eα52-68 or IAb/pigeon cytochrome c-derived analogue peptide complex. These proliferation activities were inhibited by mAb specific for IAb chain. Consistent with these findings, the emergence of NK1.1+γδ T cells was reduced in the peritoneal cavity of Aβb-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.