Elimination of CD4+CD25+ T cell accelerates the development of glomerulonephritis during the preactive phase in autoimmune-prone female NZB x NZW F1 mice
Elimination of CD4+CD25+ T cell accelerates the development of glomerulonephritis during the preactive phase in autoimmune-prone female NZB x NZW F1 mice
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DOI：
10.1111/j.0959-9673.2005.00438.x
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发表时间：
2005-10-01
影响因子：
3
通讯作者：
Adachi, C
中科院分区：
文献类型：
--
作者：
Hayashi, T;Hasegawa, K;Adachi, C
本实验在自身免疫易感的雌性NZ B x NZW F-1（B/WF 1）小鼠中研究了CD 4（+）CD 25（+）T细胞在肾小球肾炎（GN）发生发展中的作用。出生后3天给予抗小鼠CD 25（+）T细胞单克隆抗体（PC 61.5）诱导GN的发生，与未治疗的对照小鼠相比，IgG 2a抗核抗体、IL-6和IFN-γ的产生增加，而TGF-β 1的产生减少。目前的研究结果表明，在B/WF 1小鼠的活动前期，CD 4（+）CD 25（+）T细胞可能至少部分下调GN的发生。
The role of CD4(+)CD25(+) T cell in glomerulonephritis (GN) development during the preactive phase was investigated in autoimmune-prone female NZB x NZW F-1 (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-gamma, whereas TGF-beta 1 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.