Kuwana M, Kawakami Y, Ikeda Y
Institute for Advanced Medical Research, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582.
Rinsho Byori. 2001 Oct;49(10):992-5.
Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by increased platelet clearance caused by anti-platelet autoantibodies, which bind to circulating platelets resulting in destruction. by the reticuloendothelial system. We have recently developed enzyme-linked immunospot assay to detect circulating B cells secreting anti-platelet antibody. An increase in anti-platelet antibody-producing B cells in peripheral blood was specifically detected in ITP patients, but in none of thrombocytopenic patients without ITP or healthy donors. While earlier studies reported the presence of platelet-reactive T cells in ITP patients, we have recently found that GPIIb-IIIa is one of major target antigens recognized by platelet-reactive CD4+ T cells. Since GPIIb-IIIa-reactive CD4+ T cells had helper activity promoting production of anti-platelet antibody, these autoreactive T cells are involved in production of pathogenic anti-platelet autoantibody in ITP patients. Suppression of GPIIb-IIIa-reactive CD4+ T cells may be of therapeutic use in treating refractory patients.
特发性血小板减少性紫癜(ITP)是一种自身免疫性疾病,其特征是抗血小板自身抗体导致血小板清除增加,这些抗体会与循环中的血小板结合,从而被网状内皮系统破坏。我们最近开发了酶联免疫斑点测定法来检测分泌抗血小板抗体的循环B细胞。在ITP患者外周血中特异性检测到产生抗血小板抗体的B细胞增加,但在非ITP血小板减少症患者或健康供者中均未检测到。虽然早期研究报道ITP患者中存在血小板反应性T细胞,但我们最近发现糖蛋白IIb-IIIa(GPIIb-IIIa)是血小板反应性CD4+T细胞识别的主要靶抗原之一。由于GPIIb-IIIa反应性CD4+T细胞具有促进抗血小板抗体产生的辅助活性,这些自身反应性T细胞参与了ITP患者致病性抗血小板自身抗体的产生。抑制GPIIb-IIIa反应性CD4+T细胞可能对治疗难治性患者有治疗作用。