自身免疫性大疱性皮肤病细胞免疫机制进展  

Cellular immune mechanisms in autoimmune bullous derma toses

作　　者：姜蔚蔚[1] 朱英华[2] 焦阳[1] 杨敏[2] 

机构地区：[1]大连医科大学,116021 [2]大连市皮肤病医院

出　　处：《国际皮肤性病学杂志》2016年第5期417-420,共4页International Journal of Dermatology and Venereology

摘　　要：自身免疫性大疱性皮肤病是一类以皮肤、黏膜红斑和水疱为主要临床表现的皮肤病。体液免疫与细胞免疫均参与发病机制中。其中细胞免疫表现为初始T细胞通过T细胞受体与抗原特异结合后，在一些辅助因素作用下，活化、增殖并分化为效应T细胞，这些细胞表面相关细胞因子通过与B细胞表面相关受体结合，从而激发B细胞产生浆细胞及记忆细胞，进而分化为高亲和力抗体，产生免疫应答。而这些起辅助作用的细胞因子主要有辅助性T细胞、调节性T细胞等相关的细胞因子，这些细胞因子的研究对寻求自身免疫性大疱病的根源及靶向治疗意义重大。Bullous dermatoses are a class of skin diseases clinically characterized by blisters and erythema on the skin and mucous membrane. Both humoral and cellular immunity are involved in the pathogenesis of bullous dermatoses. In cellular immunity, initial T cells are activated under the effect of some cofactors after antigens specifically bind to receptors on these cells, then proliferate and differentiate into effector T cells. Subsequently, related cytokines on the surface of these effector T ceils bind to relevent receptors on the surface of B ceils to activate the B cells, followed by their differentiation into plasma ceils and memory cells, which then produce high-affinity antibodies and induce immune responses. These adjuvant cytokines are mainly related to helper T cells and regulatory T cells. Researches on these cytokines are of great significance for determining the real origin of autoimmune bullous diseases and for developing targeted therapy of them.

关 键 词：自身免疫疾病 皮肤疾病 水疱大疱性 方法 免疫 细胞因子类 

分 类 号：R758.66[医药卫生—皮肤病学与性病学]