The role of anti-HSP70 autoantibody-forming VH1-JH1 B-1 cells in Toxoplasma gondii-infected mice
Open Access
- 1 January 2003
- journal article
- research article
- Published by Oxford University Press (OUP) in International Immunology
- Vol. 15 (1) , 39-47
- https://doi.org/10.1093/intimm/dxg004
Abstract
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‐γ 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
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