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Elimination of CD4 + CD25 + T cell accelerates the development of glomerulonephritis during the preactive phase in autoimmune‐prone female NZB × NZW F 1 mice
Author(s) -
Hayashi Toshiharu,
Hasegawa Keiko,
Adachi Chie
Publication year - 2005
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.0959-9673.2005.00438.x
Subject(s) - il 2 receptor , monoclonal antibody , anti nuclear antibody , glomerulonephritis , immunology , t cell , biology , antibody , endocrinology , medicine , autoantibody , immune system , kidney
Summary The role of CD4 + CD25 + T cell in glomerulonephritis (GN) development during the preactive phase was investigated in autoimmune‐prone female NZB × NZW F 1 (B/WF 1 ) 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/WF 1 mice.