Melms A, Weissert R, Klinkert W E, Schalke B C, Tzartos S, Wekerle H
Max-Planck-Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Germany.
Neurology. 1993 Mar;43(3 Pt 1):583-8. doi: 10.1212/wnl.43.3_part_1.583.
We investigated the interaction between acetylcholine receptor (AChR)-specific T-helper cells from patients with myasthenia gravis and murine monoclonal anti-AChR antibodies. At optimal antigen concentration, anti-AChR antibodies neither enhanced nor impaired T-cell responses. However, at substimulatory antigen concentration, addition of anti-AChR antibodies substantially enhanced the proliferation of AChR-specific T cells. In spite of low amounts of antigen, immune complex formation allowed highly efficient capture and uptake of antigen via Fc receptors on antigen-presenting cells, which could be inhibited by an antibody to Fc receptors. Immune complex-mediated stimulation of sensitized AChR-specific T lymphocytes in vivo may contribute to the exacerbation of the disease, and demonstrates the interaction between T and B lymphocytes in myasthenia gravis.
我们研究了重症肌无力患者中乙酰胆碱受体(AChR)特异性辅助性T细胞与鼠单克隆抗AChR抗体之间的相互作用。在最佳抗原浓度下,抗AChR抗体既不增强也不损害T细胞反应。然而,在亚刺激抗原浓度下,添加抗AChR抗体可显著增强AChR特异性T细胞的增殖。尽管抗原量较少,但免疫复合物的形成允许通过抗原呈递细胞上的Fc受体高效捕获和摄取抗原,这可被抗Fc受体抗体抑制。免疫复合物介导的体内致敏AChR特异性T淋巴细胞刺激可能导致疾病加重,并证明了重症肌无力中T淋巴细胞与B淋巴细胞之间的相互作用。