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International Immunology, Vol. 15, No. 1, pp. 39-47, January 2003
© 2003 Japanese Society for Immunology

The role of anti-HSP70 autoantibody-forming VH1–JH1 B-1 cells in Toxoplasma gondii-infected mice

Mei Chen1, Fumie Aosai1, Kazumi Norose1, Hye-Seong Mun1 and Akihiko Yano1

1 Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan

Correspondence to: A. Yano; E-mail: yano{at}faculty.chiba-u.ac.jp.
Transmitting editor: S. Koyasu

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 VH1–JH1 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 VH1–JH1 gene, whereas the hybridoma lines producing anti-TgHSP70 antibody non-cross-reactive with mHSP70 expressed the VH11A–JH1 gene or VH12–JH1 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 VH1–JH1 mRNA, and producing anti-HSP70 autoantibody and IL-10 regulate susceptibility of mice to T. gondii infection.

Keywords: anti-HSP70 autoantibody, avidity maturation, B-1 cell, Toxoplasma gondii, VH1–JH1


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