Yoshizawa N, Oda T, Oshikawa Y, Akashi Y, Suzuki Y, Shimizu J, Shimizu E, Niwa H, Treser G
Second Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Nihon Jinzo Gakkai Shi. 1994 Apr;36(4):322-30.
To evaluate the role of cell-mediated immunity in acute poststreptococcal glomerulonephritis (APSGN), we identified the immune cell population infiltrating the glomeruli. Renal biopsies were obtained from 22 patients with APSGN, 16 with overt and 6 with asymptomatic disease, one to 30 days after onset. Samples of normal renal tissue were used as controls. Frozen sections were examined using monoclonal antibodies that recognize various leukocyte surface markers. Double staining for granulocytes and monocyte/macrophages (M phi) was performed using chloro-esterase staining and indirect immuno-alkaline-phosphatase staining with Leu M-5 sequentially. In overt APSGN, there was a substantial increase in the total number of granulocytes and M phi with a slight increase in T cells. Numbers correlated with time after onset, as more leukocytic infiltration was observed when the tissue was taken earlier. Furthermore, a significant positive linear correlation was seen between helper/inducer T cells and M phi (r = 0.86, p < 0.01). Helper T cells tended to be increased to a higher proportion during the early stage, while suppressor T cells remained constant throughout the course. Analysis with anti-proliferating cell nuclear antigen antibody revealed increased glomerular cell proliferation in the early phase of APSGN. In asymptomatic patients, the total number of leukocytes was less than in the overt patients, but the proportions of infiltrating cells were similar. These data suggest that M phi are important effector cells causing endothelial and mesangial cell proliferation in APSGN. M phi infiltration in the glomeruli appears to be mediated by complement-induced chemotaxis and probably be an antigen-specific event related to the delayed type hypersensitivity mediated by helper/inducer T cells.
为评估细胞介导的免疫在急性链球菌感染后肾小球肾炎(APSGN)中的作用,我们鉴定了浸润肾小球的免疫细胞群体。在发病后1至30天,从22例APSGN患者获取肾活检组织,其中16例为显性病例,6例为无症状病例,并以正常肾组织样本作为对照。使用识别各种白细胞表面标志物的单克隆抗体检查冰冻切片。依次使用氯酯酶染色和Leu M-5间接免疫碱性磷酸酶染色对粒细胞和单核细胞/巨噬细胞(M phi)进行双重染色。在显性APSGN中,粒细胞和M phi的总数大幅增加,T细胞略有增加。数量与发病后的时间相关,因为在更早获取组织时观察到更多的白细胞浸润。此外,辅助/诱导性T细胞与M phi之间存在显著的正线性相关性(r = 0.86,p < 0.01)。辅助性T细胞在早期往往增加到更高比例,而抑制性T细胞在整个病程中保持恒定。用抗增殖细胞核抗原抗体分析显示,APSGN早期肾小球细胞增殖增加。在无症状患者中,白细胞总数低于显性患者,但浸润细胞的比例相似。这些数据表明,M phi是导致APSGN中内皮细胞和系膜细胞增殖的重要效应细胞。肾小球中的M phi浸润似乎由补体诱导的趋化作用介导,并且可能是与辅助/诱导性T细胞介导的迟发型超敏反应相关的抗原特异性事件。