Abstract:
Behçet\'s disease (BD) is a rare inflammatory condition characterized by oral and genital ulcers, skin lesions, as well as ophthalmological, neurological, and gastrointestinal manifestations. BD involving the gastrointestinal tract is known as intestinal BD. The mucosa of the gastrointestinal tract of patients with intestinal BD exhibits enhanced levels of proinflammatory cytokines, such as IL-1β, IL-6, and TNF-α. These proinflammatory cytokines play pathogenic roles in the development of BD, as evidenced by the fact that biologics targeting these cytokines effectively induce BD remission. It should be noted, however, that the molecular mechanisms by which the blockade of these cytokines suppresses chronic inflammatory responses in BD are poorly understood. Herein, we report a case of intestinal BD resistant to prednisolone that was successfully treated with infliximab (IFX). The induction of remission by IFX was accompanied by a marked elevation of IL-6 and forkhead box P3 (FOXP3) at mRNA level. This case suggests that induction of remission by IFX is mediated not only by the suppression of TNF-α-mediated signaling pathways, but also by the promotion of IL-6 expression and accumulation of regulatory T cells expressing FOXP3.
摘要:
Behçet病(BD)是一种罕见的炎症性疾病,其特征是口腔和生殖器溃疡,皮肤损伤,以及眼科,神经学,和胃肠道表现。涉及胃肠道的BD被称为肠BD。肠道BD患者的胃肠道粘膜显示促炎细胞因子水平升高,如IL-1β,IL-6和TNF-α。这些促炎细胞因子在BD的发生发展中起着致病作用,如靶向这些细胞因子的生物制剂有效诱导BD缓解的事实证明。应该注意,然而,阻断这些细胞因子抑制BD慢性炎症反应的分子机制尚不清楚。在这里,我们报道了一例肠道BD对泼尼松龙耐药的病例,该病例成功应用英夫利昔单抗(IFX)治疗.IFX诱导缓解伴随着mRNA水平的IL-6和叉头盒P3(FOXP3)的显着升高。这种情况表明,通过IFX诱导缓解不仅通过抑制TNF-α介导的信号通路介导,还可以通过促进IL-6的表达和表达FOXP3的调节性T细胞的积累。