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类风湿关节炎(RA)是一种病因和发病机制尚不清楚的自身免疫疾病,一般认为是由多种遗传因素和环境因素共同作用的结果。遗传因素中以组织相容性白细胞抗原HLA最为重要,另外作为非HLA的肽基精氨酸脱亚胺酶4(PADI4)也参与了RA的发病。PADI4是一种翻译后修饰酶,可在钙离子存在的情况下将精氨酸残基转化为瓜氨酸残基,瓜氨酸化后的蛋白质往往改变其分子构象,从而导致其生化活性亦发生改变。在不用种族的人群中,PADI4基因多态性与RA的易感性不尽相同。PADI4在RA患者血清中含量明显升高,在机体内产生自身抗PADI4抗体,并且PADI4瓜氨酸化多种蛋白质引起机体自身的免疫反应参与RA的发生与发展。近些年来的其他研究表明PAID4也参与了肿瘤、溃疡性结肠炎、多发性硬化症的发病。尽管针对PADI4的研究已经取得了很多重大进展,但是仍然存在很多悬而未决的问题等待科研工作者进一步的研究和证实。
Rheumatoid arthritis (RA) is an autoimmune disease whose etiology and pathogenesis are not yet known and is generally thought to result from a combination of multiple genetic and environmental factors. Among the genetic factors, histocompatibility leukocyte antigen HLA is the most important, and as non-HLA peptidyl arginine deiminase 4 (PADI4) is also involved in the pathogenesis of RA. PADI4 is a post-translational modification enzyme that converts arginine residues into citrulline residues in the presence of calcium ions. Citrullinated proteins often alter their molecular conformation, resulting in their biochemical activity change. In non-ethnic populations, PADI4 genetic polymorphisms and RA susceptibility vary. PADI4 is significantly elevated in the serum of patients with RA, producing autoantibodies against PADI4 in the body, and citrullination of PADI4 causes a variety of proteins causing the body’s own immune response to participate in the development and progression of RA. Other studies in recent years have shown that PAID4 is also involved in the pathogenesis of tumors, ulcerative colitis and multiple sclerosis. Although much progress has been made in the research on PADI4, there are still many outstanding issues waiting for further research and confirmation by researchers.