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Regulatory Role of Peritoneal NK1.1⁺ß T Cells in IL-12 Production During Salmonella Infection¹

Yoshikazu Naiki^*, Hitoshi Nishimura^2,*, Tetsu Kawano, Yujiro Tanaka, Shigeyoshi Itohara, Masaru Taniguchi and Yasunobu Yoshikai^*

^* Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, and Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, Chiba, Japan; and Institute for Physical and Chemical Reseach Brain Science Institute, Saitama, Japan

NK1.1⁺ß T cells emerge in the peritoneal cavity after an i.p. infection with Salmonella choleraesuis in mice. To elucidate the role of the NK1.1⁺ß T cells during murine salmonellosis, mice lacking NK1.1⁺ß T cells by disruption of TCRß (TCRß^-/-), ß₂m (ß₂m^-/-), or J281 (J281^-/-) gene were i.p. inoculated with S. choleraesuis. The peritoneal exudate T cells in wild type (wt) mice on day 3 after infection produced IL-4 upon TCRß stimulation, whereas those in TCRß^-/-, ß₂m^-/-, or J281^-/- mice showed no IL-4 production upon the stimulation, indicating that NK1.1⁺ß T cells are the main source of IL-4 production at the early phase of Salmonella infection. Neutralization of endogenous IL-4 by administration of anti-IL-4 mAb to wt mice reduced the number of Salmonella accompanied by increased IL-12 production by macrophages after Salmonella infection. The IL-12 production by the peritoneal macrophages was significantly augmented in mice lacking NK1.1⁺ß T cells after Salmonella infection accompanied by increased serum IFN- level. The aberrantly increased IL-12 production in infected TCRß^-/- or J281^-/- mice was suppressed by adoptive transfer of T cells containing NK1.1⁺ß T cells but not by the transfer of T cells depleted of NK1.1⁺ß T cells or T cells from J281^-/- mice. Taken together, it is suggested that NK1.1⁺ß T cells eliciting IL-4 have a regulatory function in the IL-12 production by macrophages at the early phase of Salmonella infection.