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MHC Class II-Dependent NK1.1⁺ T Cells Are Induced in Mice by Salmonella Infection¹

Hitoshi Nishimura^2,*, Junji Washizu^*, Yoshikazu Naiki^*, Toru Hara^*, Yoshinori Fukui, Takehiko Sasazuki and Yasunobu Yoshikai^*

^* Laboratory of Host Defense and Germfree Life, Research Institute of Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan; and Department of Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan

We observed the emergence of a novel population of T cells expressing NK1.1 Ag in the peritoneal cavity of mice infected with Salmonella choleraesuis. The NK1.1⁺ T cells accounted for approximately 20% of all T cells emerging in the peritoneal cavity of C57BL/6 mice and expressed preferentially rearranged V4-J1 and V6.3-D1-D2-J1 genes with N diversity. The T cells proliferated vigorously in response to PHA-treated spleen cells and produced IFN- in the culture supernatant. However, spleen cells from Aß^b-deficient mice were unable to stimulate the T cells. Furthermore, the NK1.1⁺ T cells were stimulated not only by Chinese hamster ovary (CHO) cells expressing wild-type IA^b but also by those expressing IA^b/E52-68 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⁺ T cells was reduced in the peritoneal cavity of Aß^b-deficient mice after Salmonella infection, whereas NK1.1⁺ T cells were rather abundant in the peritoneal cavity of Salmonella-infected ß₂m-deficient mice. Moreover, the NK1.1⁺ T cells were easily identified in the thymus of ß₂m-deficient but not Aß^b-deficient mice. Our results indicated that MHC class II expression is essential for development and activation of NK1.1⁺ T cells in the thymus and the periphery.

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