We have previously reported that the expression of an endogenous 65-kD heat shock protein (HSP65) in macrophages is closely correlated with the protection against infection by Toxoplasma gondii in mice, and γδ T cells play a critical role in the expression of this protein. In this study, we investigated how γδ T cells contribute to the protection and HSP65 expression. After intraperitoneal infection with bradyzoites of the Beverley strain of T. gondii, mRNA encoding IFN-γ and TNF-α was detected in the peritoneal γδ T cells by RT-PCR technique, and macrophages that produced nitric oxide (NO) and expressed HSP65 were also detected. Depletion of γδ T cells resulted in suppression of NO production by macrophages, and it also inhibited HSP65 expression. HSP65 expression, however, does not appear to be induced by stimulation with NO, since treatment with NG-monomethylarginine, an inhibitor of NO synthesis, did not attenuate the expression of HSP65. This expression was completely suppressed when mice were simultaneously treated with anti-IFN-γ and anti-TNF-α although either antibody alone was less effective. The synergistic effect of these cytokines was also demonstrated by an in vitro experiment, in which peritoneal macrophages were cultured with recombinant IFN-γ and TNF-α. These results indicate that γδ T cells, which protect against infection with T. gondii induce the expression of HSP65 by secreting IFN-γ and TNF-α and the production of NO, and that the expression of HSP65 is independent of inflammatory chemical compounds like NO and H2O2.

Keywords:
Heat shock protein, Toxoplasmosis, Protective immunity, γδ T cells
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© 1996 S. Karger AG, Basel
1996
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