Role of IFN-α in Rheumatoid Arthritis

被引:7
作者
Lin, Chung M. A. [1 ,2 ]
Isaacs, John D. [1 ,2 ]
Cooles, Faye A. H. [1 ,2 ]
机构
[1] Newcastle Univ, Translat & Clin Res Inst, Newcastle Upon Tyne, England
[2] Newcastle Upon Tyne Hosp NHS Fdn Trust, Musculoskeletal Unit, Newcastle Upon Tyne, England
关键词
Rheumatoid arthritis; Early rheumatoid arthritis; Type; 1; interferons; Interferon gene signature; Biomarkers; SYSTEMIC-LUPUS-ERYTHEMATOSUS; I-INTERFERON; DENDRITIC CELLS; SYNOVIAL TISSUE; B-CELLS; EXPRESSION; SIGNATURE; DNA; TOLERANCE; RETROELEMENTS;
D O I
10.1007/s11926-023-01125-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of ReviewType 1 interferons (IFN-I) are of increasing interest across a wide range of autoimmune rheumatic diseases. Historically, research into their role in rheumatoid arthritis (RA) has been relatively neglected, but recent work continues to highlight a potential contribution to RA pathophysiology.Recent FindingsWe emphasise the importance of disease stage when examining IFN-I in RA and provide an overview on how IFN-I may have a direct role on a variety of relevant cellular functions. We explore how clinical trajectory may be influenced by increased IFN-I signalling, and also, the limitations of scores composed of interferon response genes. Relevant environmental triggers and inheritable RA genetic risk relating to IFN-I signalling are explored with emphasis on intriguing data potentially linking IFN-I exposure, epigenetic changes, and disease relevant processes.SummaryWhilst these data cumulatively illustrate a likely role for IFN-I in RA, they also highlight the knowledge gaps, particularly in populations at risk for RA, and suggest directions for future research to both better understand IFN-I biology and inform targeted therapeutic strategies.
引用
收藏
页码:37 / 52
页数:16
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