Natural recovery from antiglomerular basement membrane glomerulonephritis is associated with glomeruli-infiltrating CD8α+CD11c+MHC class II+ cells.
Natural recovery from antiglomerular basement membrane glomerulonephritis is associated with glomeruli-infiltrating CD8α+CD11c+MHC class II+ cells.
复制标题
抗肾小球基底膜肾小球肾炎的自然恢复与肾小球浸润 CD8α CD11c MHC II 类细胞有关。
DOI：
10.1159/000333004
复制
发表时间：
2011
影响因子：
4.2
通讯作者：
Lou,Ya-Huan
中科院分区：
文献类型：
--
作者：
Zhou,Cindy;Robertson,Julie;Wu,Jean;Bartkowiak,Todd;Parker,Kiana;McMahon,John;Lou,Ya-Huan
背景/目的在抗肾小球基底膜肾小球肾炎（GN）模型中，GN-抗性刘易斯（LEW）大鼠从早期肾小球炎症（21-23天）自然恢复。我们先前在GN易感的Wistar京都（WKY）大鼠中鉴定了肾小球浸润的CD 8 α+ CD 11高MHC II+细胞（GIL CD 8 α+细胞），其通过在35-40天的肾小球纤维化之前诱导T细胞凋亡来终止肾小球炎症。方法对LEW大鼠肾小球GIL CD 8 α +细胞进行定性分析，观察其浸润与T细胞凋亡的关系。结果LEW大鼠免疫后第17-22天即有GIL CD 8 α+细胞流入炎症肾小球，明显早于WKY大鼠免疫后第28-35天。值得注意的是，LEW大鼠在第17天后具有GIL CD 8 α+ CD 11高亚群，而WKY大鼠直到第30天后才缺乏该亚群。分析进一步揭示了与WKY大鼠中第35天（向纤维化转变）相比，在LEW大鼠中恢复期间（第23天）肾小球中大量聚集的凋亡CD 4+或CD 3 + T细胞。因此，GIL CD 8 α+细胞的浸润与LEW大鼠恢复期间肾小球炎症和T细胞凋亡的下降相一致。在WKY和LEW大鼠中，分离的GIL CD 8 α+细胞在20 d时均能浸润肾小球。结论GIL CD 8 α +细胞与早期肾小球炎症的恢复密切相关。这提出了GIL CD 8a+细胞参与恢复的可能性。
Background/AimsIn an antiglomerular basement membrane glomerulonephritis (GN) model, GN-resistant Lewis (LEW) rats naturally recover from early glomerular inflammation (days 21–23). We have previously identified a glomeruli-infiltrating CD8α+ CD11 high MHC II+ cell (GIL CD8α+ cell) in GN-prone Wistar Kyoto (WKY) rats, which terminates glomerular inflammation through inducing T cell apoptosis prior to glomerular fibrosis at days 35–40. We investigated if GIL CD8α+ cells were also associated with the recovery in LEW rats.MethodsGIL CD8α+ cells in LEW rats were characterized; their infiltration was observed in connection with T cell apoptosis in glomeruli.ResultsAn influx of GIL CD8α+ cells into inflamed glomeruli was confirmed in the immunized LEW rats at days 17–22, which was much earlier than days 28–35 in WKY rats. Notably, LEW rats had a GIL CD8α+ CD11 high subpopulation after day 17, while WKY rats lacked this population until after day 30. Analyses further revealed a large number of clustered apoptotic CD4+ or CD3+ T cells in the glomeruli during recovery (day 23) in LEW rats, as compared to day 35 (transition to fibrosis) in WKY rats. Thus, infiltration of GIL CD8α+ cells coincided with decline of glomerular inflammation and T cell apoptosis during recovery in LEW rats. Isolated GIL CD8α+ cells were able to infiltrate glomeruli in both WKY and LEW rats at day 20.ConclusionOur data revealed a strong association between GIL CD8a+ cells and recovery from early glomerular inflammation. It raises a possibility of involvement of GIL CD8a+ cells in the recovery.