Human Leukocyte Antigen-Disease Associations in Rheumatoid Arthritis

被引：95

作者：

van Drongelen, Vincent ^{[1
]}

Holoshitz, Joseph ^{[1
]}

机构：

[1] Univ Michigan, Dept Internal Med, 1150 West Med Ctr Dr, Ann Arbor, MI 48109 USA

来源：

RHEUMATIC DISEASE CLINICS OF NORTH AMERICA | 2017年 / 43卷 / 03期

关键词：

HLA; Rheumatoid arthritis; Autoimmunity; Shared epitope; HLA-DRB1 SHARED EPITOPE; GENE-ENVIRONMENT INTERACTION; MOLECULAR-BASIS; HISTOCOMPATIBILITY ANTIGENS; AUTOIMMUNE-DISEASES; HLA; SUSCEPTIBILITY; ANTIBODIES; SMOKING; AUTOANTIBODIES;

D O I：

10.1016/j.rdc.2017.04.003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The cause and pathogenesis of rheumatoid arthritis (RA) are influenced by environmental and genetic risk factors. Shared epitope-coding human leukocyte antigen (HLA)-DRB1 alleles increase RA risk and severity; however, the underlying mechanisms of action remain unclear. In contrast, several other DRB1 alleles protect against RA. Additionally, genome-wide association studies suggest that RA associates with other, HLA and non-HLA, genes; but the relative contributions of such risk loci to RA are incompletely understood. Future research challenges include integrating the epidemiologic and genomic data into validated arthritogenic pathways and determining the mechanisms of interaction between RA risk genes and environmental influences.

引用

页码：363 / +

页数：15

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