Casanueva B, Rodriguez-Valverde V, Fariñas M C, Vallo A, Rodriguez-Soriano J
Department of Medicine, Hospital Nacional Marqués de Valdecilla, Universidad de Santander, Spain.
Nephron. 1990;54(3):224-8. doi: 10.1159/000185859.
To assess the existence of persistent abnormalities in the cellular mechanisms regulating the immunoglobulin (Ig) synthesis in Henoch-Schönlein purpura (HSP) and IgA nephropathy, we studied through a hemolytic plaque assay (PFC) the response to the autologous mixed lymphocyte reaction (AMLR) and the T-cell suppressor activity in 24 patients with IgA nephropathy, in 20 individuals with inactive HSP (IHSP) and in 18 normal controls. In the group with IgA nephropathy there was a significant increase in the number of IgA-secreting cells after AMLR (p less than 0.01), and 9 of the 15 patients tested had an impaired generation of T-cell suppressor activity. No such abnormalities were found in individuals with IHSP. These findings support the existence of persistent defect in the mechanisms regulating the Ig synthesis, limited only to the patients with IgA nephropathy.
为评估在过敏性紫癜（HSP）和IgA肾病中调节免疫球蛋白（Ig）合成的细胞机制中持续异常的存在情况，我们通过溶血空斑试验（PFC）研究了24例IgA肾病患者、20例非活动性HSP（IHSP）个体和18名正常对照者对自体混合淋巴细胞反应（AMLR）的反应以及T细胞抑制活性。在IgA肾病组中，AMLR后分泌IgA的细胞数量显著增加（p<0.01），15例受试患者中有9例T细胞抑制活性生成受损。在IHSP个体中未发现此类异常。这些发现支持在调节Ig合成的机制中存在持续缺陷，且仅限于IgA肾病患者。
