To investigate the roles of γδ T cells in Salmonella infection, we examined the resolution of an intraperitoneal infection with avirulent Salmonella choleraesuis 31N-1 in mice lacking T-cell-receptor (TCR) α/β T cells by disruption of the TCR/β chain gene (TCRβ(-/-)). The bacteria in TCRβ(-/-) mice decreased with kinetics similar to that seen in control mice (TCRβ(+/+)) after infection. The number of natural killer (NK) cells in the peritoneal cavity increased on day 6 after infection and thereafter decreased in both TCRβ(-/-) and TCRβ(+/+) mice, whereas the number of γδ T cells, in place of αβ T cells, increased remarkably in the peritoneal cavity of TCRβ(-/-) mice on day 6 after infection. The NK cells from Salmonella- infected TCRβ(-/-) mice produced interferon-γ (IFN-γ) but neither interleukin-4 (IL-4) nor IL-13 in response to immobilized anti-NK1.1 monoclonal antibody (mAb). The γδ T cells produced IFN-γ but neither IL-4 nor IL-13 in response to heat-killed Salmonella, whereas both IFN-γ and IL- 13 but no IL-4 was produced by the γδ T cells stimulated with immobilized anti-TCR γδ mAb. In vivo administration of anti-NKl.1 mAb inhibited the reduction of Salmonella, whereas anti-TCRγδ mAb treatment did not affect the bacterial growth in TCRβ-1- mice after Salmonella infection. However, neutralization of endogenous IL-13 with anti-IL-13 mAb enhanced the bacterial clearance in TCRβ(-/-) mice after infection. These results suggest that NKI.1 + cells serve mainly to protect against avirulent Salmonella infection in the absence of αβ T cells, whereas γδ T cells may play dichotomous roles in Salmonella infection through IFN-γ and IL-13 in TCRβ-1- mice.(C) 2000 Academic Press.
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