Institute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Germany.
Clin Pharmacol Ther. 2017 Oct;102(4):564-567. doi: 10.1002/cpt.792.
There is an increasing understanding on the etiology of chronic immune-mediated inflammatory diseases such as inflammatory bowel disease (IBD), psoriasis, or rheumatoid arthritis. Large consortia contributed to the elucidation of the genetics, for instance, of IBD identifying a number of genes involved in innate mucosal defense and immune tolerance (most prominent, e.g., NOD2) and other related processes. For a number of such diseases, common genetic susceptibility loci were identified, suggesting overlapping immune response pathways, although there is no causality of single genetic traits. In particular, the elucidation of main triggers of inflammation like tumor necrosis factor alpha (TNFα), integrins, specific cytokines like interleukin (IL)-6 or IL-23 launched the successful development of new pharmacological approaches, leading to a tremendous improvement of therapeutic outcomes.
人们对慢性免疫介导的炎症性疾病（如炎症性肠病、银屑病或类风湿关节炎）的病因有了越来越多的认识。大型研究联盟为阐明遗传学做出了贡献，例如，炎症性肠病的遗传学确定了许多参与先天黏膜防御和免疫耐受的基因（最突出的是 NOD2）和其他相关过程。对于许多此类疾病，已经确定了常见的遗传易感性位点，表明存在重叠的免疫反应途径，尽管单个遗传特征没有因果关系。特别是，阐明肿瘤坏死因子-α（TNFα）、整合素等主要炎症触发物，以及白细胞介素（IL）-6 或 IL-23 等特定细胞因子，为新的药理学方法的成功开发奠定了基础，从而极大地改善了治疗效果。
