Elimination of CD4+CD25+ T cell accelerates the development of glomerulonephritis during the preactive phase in autoimmune-prone female NZB × NZW F1 mice

Authors

  • Toshiharu Hayashi,

    Corresponding author
    1. Laboratory of Veterinary Pathology, Faculty of Agriculture, Yamaguchi University, Yoshida, Yamaguchi, Japan
      T. Hayashi
      Laboratory of Veterinary Pathology
      Faculty of Agriculture
      Yamaguchi University
      1677-1, Yoshida
      Yamaguchi 753-8515
      Japan
      Tel.: +44 81 83 933 5890
      Fax: +44 81 83 933 5890
      E-mail: hayasi@yamaguchi-u.ac.jp
    Search for more papers by this author
  • Keiko Hasegawa,

    1. Laboratory of Veterinary Pathology, Faculty of Agriculture, Yamaguchi University, Yoshida, Yamaguchi, Japan
    Search for more papers by this author
  • Chie Adachi

    1. Laboratory of Veterinary Pathology, Faculty of Agriculture, Yamaguchi University, Yoshida, Yamaguchi, Japan
    Search for more papers by this author

T. Hayashi
Laboratory of Veterinary Pathology
Faculty of Agriculture
Yamaguchi University
1677-1, Yoshida
Yamaguchi 753-8515
Japan
Tel.: +44 81 83 933 5890
Fax: +44 81 83 933 5890
E-mail: hayasi@yamaguchi-u.ac.jp

Summary

The role of CD4+CD25+ T cell in glomerulonephritis (GN) development during the preactive phase was investigated in autoimmune-prone female NZB × NZW F1 (B/WF1) mice. The administration of anti-mouse CD25+ T-cell monoclonal antibody (PC61.5) 3 days after birth induced the development of GN with an increase in IgG2a antinuclear antibody, productions of IL-6 and IFN-γ, whereas TGF-β1 production decreased, compared to untreated control mice. The present study results suggest that CD4+CD25+ T cells may, at least in part, downregulate the development of GN during the preactive phase in B/WF1 mice.

Ancillary