Tipping P G, Neale T J, Holdsworth S R
Kidney Int. 1985 Mar;27(3):530-7. doi: 10.1038/ki.1985.43.
Macrophage accumulation is a feature of some aggressive forms of human and experimental glomerulonephritis (GN). Both antibody Fc components and T cells may cause macrophage accumulation; however, there has been no previous demonstration of T cells at the site of injury in GN, although some indirect evidence of their possible participation has been reported. Specific monoclonal anti-rat T lymphocyte antibodies W3/13, W3/25, and Ox8 were used to demonstrate T cells within the glomeruli of rats with an augmented autologous anti-GBM GN, by indirect immunofluorescence. The injury in this model has been shown to be mediated by macrophages. The T cell infiltrate consisted mainly of T helper cells, was maximal 24 hr after induction of the disease and clearly preceded the peak influx of macrophages and glomerular damage. Suppression of T cell function using cyclosporin prevented T cell accumulation and the subsequent macrophage-induced injury. Glomerular T cells were not seen in passively induced GN. These studies support a role for cell-mediated immunity in attracting macrophages and initiating injury in experimental anti-GBM antibody-induced GN.
巨噬细胞聚集是某些侵袭性人类和实验性肾小球肾炎（GN）的一个特征。抗体Fc成分和T细胞都可能导致巨噬细胞聚集；然而，此前在GN损伤部位尚未证实有T细胞存在，尽管已有一些关于它们可能参与的间接证据报道。通过间接免疫荧光法，使用特异性单克隆抗大鼠T淋巴细胞抗体W3/13、W3/25和Ox8来证实患有自体抗肾小球基底膜（GBM）增强型GN的大鼠肾小球内存在T细胞。该模型中的损伤已被证明是由巨噬细胞介导的。T细胞浸润主要由辅助性T细胞组成，在疾病诱导后24小时达到最大值，且明显先于巨噬细胞的最大流入量和肾小球损伤。使用环孢素抑制T细胞功能可防止T细胞聚集以及随后由巨噬细胞诱导的损伤。在被动诱导的GN中未观察到肾小球T细胞。这些研究支持细胞介导的免疫在吸引巨噬细胞和引发实验性抗GBM抗体诱导的GN损伤中发挥作用。
