The genetic pathogenesis, diagnosis and therapeutic insight of rheumatoid arthritis

被引:41
|
作者
Zamanpoor, Mansour [1 ,2 ]
机构
[1] Univ Otago, Dept Biochem, Dunedin, New Zealand
[2] Wellington Reg Hosp, Genet Hlth Serv New Zealand, Wellington Reg Genet Lab, Private Bag 7902, Wellington 6242, New Zealand
关键词
Rheumatoid Arthritis; Genetic; Pathogenesis; GWAS; HLA; GENOME-WIDE ASSOCIATION; TYROSINE-PHOSPHATASE PTPN22; VITAMIN-D; SHARED EPITOPE; CITRULLINATED PEPTIDE; FC RECEPTOR-LIKE-3; JAPANESE PATIENTS; INCREASED RISK; STAT4; GENE; T-CELLS;
D O I
10.1111/cge.13498
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Rheumatoid arthritis (RA) is a systemic autoimmune disease that causes chronic inflammation of the joints. RA is a heterogeneous disorder caused by an abnormal autoimmune response triggered by the complex interactions of genetic and environmental factors that contribute to RA etiology. However, its underlying pathogenic mechanisms are yet to be fully understood. In this review, I provide an overview of the pathogenesis, diagnosis and therapeutic insight in the clinical management of RA in light of the recent updates to classification criteria and recent discoveries of genetic loci associated with susceptibility for RA.
引用
收藏
页码:547 / 557
页数:11
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