The role of anti-HSP70 autoantibody-forming V(H)1-J(H)1 B-1 cells in Toxoplasma gondii-infected mice.

Anti-heat shock protein 70 (HSP70) autoantibody formation was induced by B-1 cells (CD5(+) B cells) in Toxoplasma gondii-infected mice. Here we report that V(H)1-J(H)1 B-1 cells from peritoneal exudate cells (PEC) of T. gondii-infected C57BL/6 mice (B6, a susceptible strain) increased predominantly. Moreover, the hybridoma lines producing anti-T. gondii HSP70 (TgHSP70) antibody cross-reactive with mouse HSP70 (mHSP70) expressed the V(H)1-J(H)1 gene, whereas the hybridoma lines producing anti-TgHSP70 antibody non-cross-reactive with mHSP70 expressed the V(H)11A-J(H)1 gene or V(H)12-J(H)1 gene. The avidity maturation of anti-TgHSP70 IgG antibody in the sera of BALB/c mice (a resistant strain) and that of anti-mHSP70 IgG autoantibody in the sera of B6 mice were observed 9 weeks after T. gondii infection. T. gondii numbers in the brains of T. gondii-infected B6 mice treated with anti-mHSP70 autoantibody were markedly higher than those in the brains of T. gondii-infected B6 mice treated with anti-TgHSP70 antibody. Furthermore, B-1 cells producing IL-10 down-regulated the IFN-gamma expression of PEC in T. gondii-infected mice. These results indicate that B-1 cells dominantly expressing V(H)1-J(H)1 mRNA, and producing anti-HSP70 autoantibody and IL-10 regulate susceptibility of mice to T. gondii infection.