Bania M B, Antel J P, Reder A T, Nicholas M K, Arnason B G
J Clin Invest. 1986 Aug;78(2):582-6. doi: 10.1172/JCI112612.
Patients with progressive multiple sclerosis (MS) demonstrated persistent reductions in levels of concanavalin A (Con A)-induced suppressor activity and heightened levels of in vitro pokeweed mitogen (PWM)-induced IgG secretion. The reduced Con A suppressor activity could not be reversed by addition of interleukin 2 (IL-2). Cyclosporine A (CsA) treatment did not alter the defect in Con A-induced suppressor activity, but did markedly inhibit T8+ cell-mediated alloantigen directed cytolytic activity; this latter defect was reversible by in vitro addition of IL-2. CsA-treated patients did not differ from placebo-treated patients with regard to levels of PWM-induced IgG secretion or proliferative responses of their mononuclear cells to Con A. The results indicate that CsA treatment of MS patients reduces cytolytic function from baseline normal values, but does not alter aberrant suppressor cell function.
进行性多发性硬化症（MS）患者表现出伴刀豆球蛋白A（Con A）诱导的抑制活性水平持续降低，以及体外商陆有丝分裂原（PWM）诱导的IgG分泌水平升高。添加白细胞介素2（IL-2）无法逆转Con A抑制活性的降低。环孢素A（CsA）治疗并未改变Con A诱导的抑制活性缺陷，但显著抑制了T8 +细胞介导的同种异体抗原定向细胞溶解活性；后一种缺陷可通过体外添加IL-2逆转。在PWM诱导的IgG分泌水平或其单核细胞对Con A的增殖反应方面，CsA治疗的患者与安慰剂治疗的患者没有差异。结果表明，CsA治疗MS患者可使细胞溶解功能从基线正常值降低，但不会改变异常的抑制细胞功能。
