HLA-B27与强直性脊柱炎免疫学机制的研究进展  

Advance of Research on HLA-B27 and the Immunological Mechanism of Ankylosing Spondylitis

作　　者：李梦远[1] 姚中强[1] 刘湘源[1] 

机构地区：[1]北京大学第三医院风湿免疫科,北京100191

出　　处：《生理科学进展》2011年第1期16-20,共5页Progress in Physiological Sciences

摘　　要：强直性脊柱炎是与HLA-B27有明确相关性的自身免疫性疾病,其发病过程包括了微生物和宿主的相互作用、免疫细胞对MHC-Ⅰ类分子的识别以及细胞因子网络的失平衡等方面。未折叠蛋白应答反应参与了强直性脊柱炎发病过程,并且下游IL-23/IL-17轴的激活可能在发病过程中起重要作用。未折叠蛋白反应和IL-23/IL-17轴是研究强直性脊柱炎发病机制和防治措施的新靶点。Ankylosing spondylitis（AS） is an autoimmune disease which has a strong association with HLA-B27.Its pathogenesis includes the interaction between microorganism and host,the recognition of MHC class Ⅰ molecule by immune cells and the imbalance of the cytokine network and so on.Unfolded protein response（UPR） participates in the development of AS.And the activation of the IL-23/IL-17 axis,which is in the downstream of UPR,may make a critical contribution to the pathogenesis.UPR and IL-23/IL-17 axis open new avenues of investigation as well as identifying new therapeutic target in this disease.

关 键 词：HLA-B27 强直性 脊柱炎 未折叠蛋白应答 

分 类 号：R363.2[医药卫生—病理学] R593.23[医药卫生—基础医学]