III Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20246 Hamburg, Germany.
J Mol Med (Berl). 2010 Jan;88(1):19-26. doi: 10.1007/s00109-009-0541-5. Epub 2009 Oct 2.
T cells have long been suspected to contribute to glomerulonephritis not only as helpers for antibody-producing B cells, but also as immune effector cells. Recent evidence has substantiated this hypothesis, by identifying tubulointerstitial dendritic cells (DCs) as crucial interaction partners. Kidney DCs capture glomerular antigens released for example by cytotoxic CD8(+) T cells and present them to infiltrating CD4(+) T helper cells. This cross-talk results in the production of proinflammatory cytokines and chemokines that recruit and activate further immune effector cells. Such immunocytes are the main components of the well-known tubulointerstitial mononuclear infiltrate characteristic of progressive renal disease. These findings indicate that effector T cell dysregulation by intrarenal DCs and by the chemokines they produce represents a hitherto unknown mechanism by which glomerular damage can cause chronic tubulointerstitial inflammation.
T 细胞长期以来一直被怀疑不仅作为产生抗体的 B 细胞的辅助细胞，而且作为免疫效应细胞，有助于肾小球肾炎的发生。最近的证据证实了这一假说，通过鉴定肾小管间质树突状细胞 (DC) 作为关键的相互作用伙伴。肾脏 DC 捕获例如由细胞毒性 CD8(+) T 细胞释放的肾小球抗原，并将其呈递给浸润的 CD4(+) T 辅助细胞。这种串扰导致产生促炎细胞因子和趋化因子，募集并激活更多的免疫效应细胞。这种免疫细胞是进展性肾脏疾病特征性的肾小管间质单核细胞浸润的已知成分。这些发现表明，肾内 DC 产生的趋化因子导致效应 T 细胞失调，代表了一种未知的机制，即肾小球损伤可导致慢性肾小管间质炎症。
