MHC class II-dependent NK1.1(+) gamma delta T cells are induced in mice bySalmonella infection

We observed the emergence of a novel population of gamma delta T cells expr essing NK1.1 Ag in the peritoneal cavity of mice infected with Salmonella c holeraesuis. The NK1.1(+) gamma delta T cells accounted for approximately 2 0% of all gamma delta T cells emerging in the peritoneal cavity of C57BL/6 mice and expressed preferentially rearranged V gamma 4-J gamma 1 and V delt a 6.3-D delta 1-D delta 2-J delta 1 genes with N diversity. The gamma delta T cells proliferated vigorously in response to PHA-treated spleen cells an d produced IFN-gamma in the culture supernatant, However, spleen cells from A beta(b)-deficient mice were unable to stimulate the gamma delta T cells. Furthermore, the NK1.1(+)gamma delta T cells were stimulated not only by C hinese hamster ovary (CHO) cells expressing wild-type IA(b) but also by tho se expressing IA(b)/E alpha 52-68 or IA(b)/pigeon cytochrome c-derived anal ogue peptide complex. These proliferation activities were inhibited by mAb specific for IA(b) chain. Consistent,vith these findings, the emergence of NK1.1(+) gamma delta T cells was reduced in the peritoneal cavity of A beta (b)-deficient mice after Salmonella infection, whereas NK1.1(+)gamma delta T cells were rather abundant in the peritoneal cavity of Salmonella-infecte d beta(2)m-deficient mice. Moreover, the NK1.1(+)gamma delta T cells were e asily identified in the thymus of beta(2)m-deficient but not A beta(b)-defi cient mice. Our results indicated that MHC class II expression is essential for development and activation of NK1.1(+)gamma delta T cells in the thymu s and the periphery.