gammadelta T cells may dichotomously modulate infection with avirulent Salmonella choleraesuis via IFN-gamma and IL-13 in mice.
To investigate the roles of gammadelta 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) alphabeta T cells by disruption of the TCRbeta chain gene (TCRbeta(-/-)). The bacteria in TCRbeta(-/-) mice decreased with kinetics similar to that seen in control mice (TCRbeta(+/+)) after infection. The number of natural killer (NK) cells in the peritoneal cavity increased on day 6 after infection and thereafter decreased in both TCRbeta(-/-) and TCRbeta(+/+) mice, whereas the number of gammadelta T cells, in place of alphabeta T cells, increased remarkably in the peritoneal cavity of TCRbeta(-/-) mice on day 6 after infection. The NK cells from Salmonella-infected TCRbeta(-/-) mice produced interferon-gamma (IFN-gamma) but neither interleukin-4 (IL-4) nor IL-13 in response to immobilized anti-NK1.1 monoclonal antibody (mAb). The gammadelta T cells produced IFN-gamma but neither IL-4 nor IL-13 in response to heat-killed Salmonella, whereas both IFN-gamma and IL-13 but no IL-4 was produced by the gammadelta T cells stimulated with immobilized anti-TCRgammadelta mAb. In vivo administration of anti-NK1.1 mAb inhibited the reduction of Salmonella, whereas anti-TCRgammadelta mAb treatment did not affect the bacterial growth in TCRbeta(-/-) mice after Salmonella infection. However, neutralization of endogenous IL-13 with anti-IL-13 mAb enhanced the bacterial clearance in TCRbeta(-/-) mice after infection. These results suggest that NK1.1(+) cells serve mainly to protect against avirulent Salmonella infection in the absence of alphabeta T cells, whereas gammadelta T cells may play dichotomous roles in Salmonella infection through IFN-gamma and IL-13 in TCRbeta(-/-) mice.
Naiki
Y
Y
Laboratory of Host Defense and Germ-free Life, Nagoya University School of Medicine, Nagoya, 466-0053, Japan.
Nishimura
H
H
Itohara
S
S
Yoshikai
Y
Y
D000818:Animals; D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D005122:Exudates and Transudates; D005260:Female; D019674:Genes, T-Cell Receptor beta; D007371:Interferon-gamma / Q000276:immunology*; D018793:Interleukin-13 / Q000276:immunology*; D037181:Lectins, C-Type; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D055651:NK Cell Lectin-Like Receptor Subfamily B; D010537:Peritoneum / Q000276:immunology; D011506:Proteins; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics; D012475:Salmonella / Q000472:pathogenicity*; D012481:Salmonella Infections, Animal / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D000941:Antigens; D000950:Antigens, Ly; D000954:Antigens, Surface; D018793:Interleukin-13; C527211:Klrb1c protein, mouse; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D011506:Proteins; D016692:Receptors, Antigen, T-Cell, gamma-delta; D007371:Interferon-gamma