Interplay between TLR-mediated innate immunity, acquired immunity and in Toxoplasma gondii-derived heat shock protein, TgHSP70, in toxoplasmosis

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Anti-heat shock 70 (HSP70) autoantibody formation was induced by VH1-JH1 B-1 cells (CD5^+ B cells) in Toxoplasma gondii-infected mice. B-1 cell producing anti-HSP70 autoantibody down-regulated host immune responses. T.gondii-derived HSP70 (TgHSP70) activated B cells via Toll-like receptor(TLR) 4, and also inhibited No production by T.godii-infected macrophages via TLR2. MyD88 (an adaptor of TLR for signal transduction) KO mice were shown to be susceptible to even small numbers of T.gondii cysts per oral(p.o.) infection, and TLR2 KO mice were shown to be susceptible to high dose cysts p.o. infection. The damage of kidney from TLR4-deficient mice was less severe compared to TLR2-deficient mice, and histopathological damage of the kidney was not observed in wild type mice. Thus TLR2 plays a role in the protection of the renal function against T.gondii infection. Wild type and TLR4 KO mice were shown to be resistant to T.gondii infection. Furthermore, T.gondii infection inhibited the development of lupus-like syndrome in autoimmune (New Zealand Black x New Zealand White) F1 mice. Over all, these data indicate that there exist tight correlation between TgHSP70 derived from T.gondii, TLR-mediated innate immunity, and B cell-mediated acquired immunity, and immuno-regulatory role of T.gondii in an autoimmune systematic erythematodes (SLE) murine model.