The pathogenesis of rheumatoid arthritis

被引：297

作者：

Alivernini, Stefano ^{[1
,2
]}

Firestein, Gary S. ^{[3
]}

McInnes, Iain B. ^{[4
]}

机构：

[1] Fdn Policlin Univ A Gemelli IRCCS, Immunol Res Core Facil, Gemelli Sci & Technol Pk, Rome, Italy

[2] Univ Cattolica Sacro Cuore, Div Rheumatol, Fdn Policlin Univ A Gemelli IRCCS, Rome, Italy

[3] Univ Calif San Diego, Sch Med, Div Rheumatol Allergy & Immunol, La Jolla, CA 92093 USA

[4] Univ Glasgow, Coll MVLS, Glasgow, Scotland

来源：

IMMUNITY | 2022年 / 55卷 / 12期

关键词：

FIBROBLAST-LIKE SYNOVIOCYTES; ANTICITRULLINATED PROTEIN ANTIBODIES; NICOTINIC ACETYLCHOLINE-RECEPTOR; POSITIVE T-CELLS; SYNOVIAL FIBROBLASTS; DNA METHYLATION; INFLAMMATORY ARTHRITIS; CYTOKINE PRODUCTION; PEPTIDE ANTIBODY; DISEASE SEVERITY;

D O I：

10.1016/j.immuni.2022.11.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

Significant recent progress in understanding rheumatoid arthritis (RA) pathogenesis has led to improved treatment and quality of life. The introduction of targeted-biologic and -synthetic disease modifying antirheumatic drugs (DMARDs) has also transformed clinical outcomes. Despite this, RA remains a life-long disease without a cure. Unmet needs include partial response and non-response to treatment in many patients, failure to achieve immune homeostasis or drug free remission, and inability to repair damaged tissues. RA is now recognized as the end of a multi-year prodromal phase in which systemic immune dysregulation, likely beginning in mucosal surfaces, is followed by a symptomatic clinical phase. Inflammation and immune reactivity are primarily localized to the synovium leading to pain and articular damage, but is also associated with a broader series of comorbidities. Here, we review recently described immunologic mechanisms that drive breach of tolerance, chronic synovitis, and remission.

引用

页码：2255 / 2270

页数：16

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