Nakagawa T Y, Brissette W H, Lira P D, Griffiths R J, Petrushova N, Stock J, McNeish J D, Eastman S E, Howard E D, Clarke S R, Rosloniec E F, Elliott E A, Rudensky A Y
Howard Hughes Medical Institute, and Department of Immunology, University of Washington School of Medicine, Seattle 98115, USA.
Immunity. 1999 Feb;10(2):207-17. doi: 10.1016/s1074-7613(00)80021-7.
Cathepsins have been implicated in the degradation of proteins destined for the MHC class II processing pathway and in the proteolytic removal of invariant chain (Ii), a critical regulator of MHC class II function. Mice lacking the lysosomal cysteine proteinase cathepsin S (catS) demonstrated a profound inhibition of Ii degradation in professional APC in vivo. A marked variation in the generation of MHC class II-bound Ii fragments and presentation of exogenous proteins was observed between B cells, dendritic cells, and macrophages lacking catS. CatS-deficient mice showed diminished susceptibility to collagen-induced arthritis, suggesting a potential therapeutic target for regulation of immune responsiveness.
组织蛋白酶与主要组织相容性复合体(MHC)II类加工途径中蛋白质的降解以及MHC II类功能的关键调节因子恒定链(Ii)的蛋白水解去除有关。缺乏溶酶体半胱氨酸蛋白酶组织蛋白酶S(catS)的小鼠在体内的专职抗原呈递细胞(APC)中表现出对Ii降解的显著抑制。在缺乏catS的B细胞、树突状细胞和巨噬细胞之间,观察到MHC II类结合的Ii片段生成和外源蛋白呈递存在显著差异。缺乏catS的小鼠对胶原诱导的关节炎的易感性降低,这表明catS是调节免疫反应性的一个潜在治疗靶点。