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大动脉炎为一类机制不明的非特异性大血管炎,既往研究提示遗传因素参与其发病。人类白细胞抗原(HLA)-B~*52:01是唯一不同种族重复验证的大动脉炎易感基因,与主动脉瓣反流密切相关。HLA-B52抗原肽结合区的第67位氨基酸是大动脉炎特异性抗原表位,呈递内源性抗原后启动大动脉炎。HLA-B67、HLA-B/MICA基因是新发现的大动脉炎易感基因。大动脉炎中65-KD HSP及TNF-α分别通过HSE通路及NK-kB通路促使MICA表达上调,触发急性血管壁炎症。HLAⅡ类基因区的易感基因与种族背景相关,多以单倍型出现。HLA-DPB1~*09、HLA-DRB1~*07、HLA-DQB1~*06:01是中国人群大动脉炎易感基因。FCGR2A/FCGR3A基因可能参与的体液免疫加速大动脉炎进程。IL12B基因介导的Th1及Th17细胞通路是大动脉炎适应性免疫应答的重要机制,提示大动脉炎未来治疗方向。
Arteritis is a type of unknown mechanism of non-specific major vasculitis, past studies suggest that genetic factors involved in the pathogenesis. Human Leukocyte Antigen (HLA) -B ~ * 52: 01 is the only genetically diverse aortic artery susceptibility gene that is closely related to aortic regurgitation. The amino acid at position 67 of the HLA-B52 antigen peptide binding region is a polyarteritis-specific epitope, which is presented after the endogenous antigen is presented. HLA-B67, HLA-B / MICA genes are newly discovered aortic arteritis susceptibility genes. Atherosclerosis in the 65-KD HSP and TNF-α, respectively, through the HSE pathway and NK-kB pathway to promote MICA expression, triggering acute vascular wall inflammation. HLA class II gene region susceptibility genes and ethnic background, mostly haplotype. HLA-DPB1 ~ * 09, HLA-DRB1 ~ * 07, HLA-DQB1 ~ * 06: 01 are Chinese aorta inflammation susceptibility genes. Humoral immunity accelerated by the FCGR2A / FCGR3A gene may accelerate the process of aorta inflammation. IL12B gene-mediated Th1 and Th17 cell pathways is an important mechanism of adaptive immune response of arteritis, suggesting the future treatment of arteritis.