Boyce N W, Tipping P G, Holdsworth S R
Kidney Int. 1986 Nov;30(5):673-7. doi: 10.1038/ki.1986.239.
Glomerular T-lymphocyte infiltration has recently been demonstrated to precede glomerular macrophage influx in a pre-immunized model of anti-glomerular basement-membrane antibody-induced glomerulonephritis (antiGBM-GN). In the current study, the functional role of these glomerular T-lymphocytes in directing macrophage localization was sought by measuring their production of macrophage migration inhibition factor (MIF). MIF activity in supernatants from cultured isolated glomeruli was measured in a conventional capillary tube bioassay. Glomerular T-lymphocytes (OX19 positive cells) were maximal (1.95 +/- 0.19 cells/glomerular cross section, c/gcs) 24 hours after injection of antiGBM antibody into sensitized animals. Seventy-two hours after antibody injection, T-lymphocyte numbers were reduced (1.02 +/- 0.14 c/gcs) while macrophage accumulation was maximal (at 24 hrs 4.2 +/- 1.3 macrophages/glomerulus (m/g), at 72 hrs 19.8 +/- 3.7 m/g). MIF activity was only detected in supernatants from T-lymphocyte infiltrated glomeruli (12 hrs 40.81 +/- 4.32% migration inhibition, 24 hrs 45.11 +/- 4.11% migration inhibition, 48 hrs 38.24 +/- 3.53% migration inhibition, 72 hrs 20.86 +/- 3.85% migration inhibition, all P less than 0.05). Control glomeruli from normal animals, pre-immunized animals given normal sheep globulin, pre-immunized animals given anti-GBM antibody and Cyclosporin A, and non-pre-immunized animals given antiGBM antibody did not contain glomerular T-lymphocytes, and their supernatants contained no MIF activity. This data indicates that the glomerular T-lymphocytes in pre-immunized antiGBM-GN are sensitized cells which release MIF and thus may direct glomerular macrophage localization in this model of antibody-induced glomerulonephritis.
在抗肾小球基底膜抗体诱导的肾小球肾炎（抗GBM - GN）的预免疫模型中，最近已证明肾小球T淋巴细胞浸润先于肾小球巨噬细胞流入。在当前研究中，通过测量肾小球T淋巴细胞产生的巨噬细胞迁移抑制因子（MIF）来探寻这些肾小球T淋巴细胞在指导巨噬细胞定位中的功能作用。采用传统的毛细管生物测定法测量培养的分离肾小球上清液中的MIF活性。向致敏动物注射抗GBM抗体后24小时，肾小球T淋巴细胞（OX19阳性细胞）数量达到最大值（1.95±0.19个细胞/肾小球横截面，c/gcs）。抗体注射72小时后，T淋巴细胞数量减少（1.02±0.14 c/gcs），而巨噬细胞积累达到最大值（24小时时为4.2±1.3个巨噬细胞/肾小球（m/g），72小时时为19.8±3.7 m/g）。仅在T淋巴细胞浸润的肾小球上清液中检测到MIF活性（12小时时迁移抑制率为40.81±4.32%，24小时时为45.11±4.11%，48小时时为38.24±3.53%，72小时时为20.86±3.85%，所有P均小于0.05）。来自正常动物、接受正常羊球蛋白的预免疫动物、接受抗GBM抗体和环孢素A的预免疫动物以及接受抗GBM抗体的未预免疫动物的对照肾小球不含肾小球T淋巴细胞，其上清液也不含MIF活性。该数据表明，预免疫的抗GBM - GN中的肾小球T淋巴细胞是释放MIF的致敏细胞，因此在这种抗体诱导的肾小球肾炎模型中可能指导肾小球巨噬细胞的定位。
