Sakai H
Department of Internal Medicine, School of Medicine, Tokai University, Isehara City, Japan.
Am J Kidney Dis. 1988 Nov;12(5):430-2. doi: 10.1016/s0272-6386(88)80040-4.
Polyclonal activation of IgA-producing B cells has been observed in the majority of patients with IgA nephropathy (IgAN) and some of their family members. The precise mechanism of such activation is presently unknown. However, abnormalities of T and B cell interactions have recently been observed in this disease. These abnormalities include the decrease of IgA-specific suppressor T cell activity and the increase of IgA-specific helper T cell activity. A T cell subpopulation with receptors for the Fc portion of IgA and with CD4 antigens (ie, T alpha 4 cells) has been proposed as a candidate of IgA-specific switch T cells that convert IgM-producing B cells to IgA-producing B cells. Further analysis of the immunogenetic mechanism and the clinical correlates of the cellular immunoregulatory aspects of IgAN is necessary to elucidate the pathogenesis of this disease.
在大多数IgA肾病（IgAN）患者及其部分家庭成员中，已观察到产生IgA的B细胞的多克隆激活。目前尚不清楚这种激活的确切机制。然而，最近在这种疾病中观察到了T细胞和B细胞相互作用的异常。这些异常包括IgA特异性抑制性T细胞活性降低和IgA特异性辅助性T细胞活性增加。一种具有IgA Fc部分受体和CD4抗原的T细胞亚群（即Tα4细胞）已被提出作为将产生IgM的B细胞转化为产生IgA的B细胞的IgA特异性转换T细胞的候选者。进一步分析IgAN的免疫遗传机制及其细胞免疫调节方面的临床相关性，对于阐明该疾病的发病机制是必要的。
