Bennett A, Frampton G, Cameron J S
Br J Haematol. 1986 Apr;62(4):695-703. doi: 10.1111/j.1365-2141.1986.tb04093.x.
We studied platelet-associated IgG (PAIgG) in patients with the nephritis of systemic lupus erythematosus (SLE) and with idiopathic glomerulonephritis (IGN), and found no increase in PAIgG in the patients with IGN, and an increase in only a minority of patients with SLE, all of whom had active disease. Patients with IGN and a nephrotic syndrome had both a low serum IgG and a low PAIgG. The increase in PAIgG in the patients with SLE correlated with the titres of antibody against dsDNA in the serum, but not with the platelet-agglutinating immune complexes also present. Intraplatelet serotonin, however, was reduced in both groups, and this correlated with the amounts of platelet-agglutinating complexes in the serum of the SLE patients. Immune complexes may associate with platelets in vivo to cause this release, but if so this must be a reversible phenomenon ('hit and run' immune platelet injury); alternatively, the Fc binding to the platelet surface may be weak and insufficient to survive the ex vivo washing procedures.
我们研究了系统性红斑狼疮(SLE)肾炎患者和特发性肾小球肾炎(IGN)患者的血小板相关IgG(PAIgG),发现IGN患者的PAIgG没有增加,而SLE患者中只有少数患者的PAIgG增加,且所有这些患者都患有活动性疾病。患有IGN和肾病综合征的患者血清IgG和PAIgG均较低。SLE患者PAIgG的增加与血清中抗双链DNA抗体的滴度相关,但与同时存在的血小板凝集免疫复合物无关。然而,两组患者的血小板内5-羟色胺均减少,这与SLE患者血清中血小板凝集复合物的量相关。免疫复合物可能在体内与血小板结合导致这种释放,但如果是这样,这一定是一种可逆现象(“打了就跑”的免疫性血小板损伤);或者,Fc与血小板表面的结合可能较弱,不足以在体外洗涤过程中存活。