Driving chronicity in rheumatoid arthritis: perpetuating role of myeloid cells

被引：36

作者：

Alivernini, S. ^{[1
]}

Tolusso, B. ^{[1
]}

Ferraccioli, G. ^{[1
]}

Gremese, E. ^{[1
]}

Kurowska-Stolarska, M. ^{[2
,3
]}

McInnes, I. B. ^{[2
,3
]}

机构：

[1] Univ Cattolica Sacro Cuore, Inst Rheumatol, Fdn Policlin Univ A Gemelli, Rome, Italy

[2] Univ Glasgow, Inst Infect Immun & Inflammat, 120 Univ Pl, Glasgow G12 8TA, Lanark, Scotland

[3] Rheumatoid Arthrit Pathogenesis Ctr Excellence RA, Glasgow, Lanark, Scotland

来源：

CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2018年 / 193卷 / 01期

关键词：

arthritis (including rheumatoid arthritis); cytokines; inflammation; macrophage; COLONY-STIMULATING FACTOR; NECROSIS-FACTOR-ALPHA; GM-CSF RECEPTOR; CARTILAGE PANNUS JUNCTION; HUMAN MONOCLONAL-ANTIBODY; REGULATORY T-CELLS; TOLL-LIKE RECEPTOR; DENDRITIC CELLS; SYNOVIAL FIBROBLASTS; INFLAMMATORY ARTHRITIS;

D O I：

10.1111/cei.13098

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Acute inflammation is a complex and tightly regulated homeostatic process that includes leucocyte migration from the vasculature into tissues to eliminate the pathogen/injury, followed by a pro-resolving response promoting tissue repair. However, if inflammation is uncontrolled as in chronic diseases such as rheumatoid arthritis (RA), it leads to tissue damage and disability. Synovial tissue inflammation in RA patients is maintained by sustained activation of multiple inflammatory positive-feedback regulatory pathways in a variety of cells, including myeloid cells. In this review, we will highlight recent evidence uncovering biological mechanisms contributing to the aberrant activation of myeloid cells that contributes to perpetuation of inflammation in RA, and discuss emerging data on anti-inflammatory mediators contributing to sustained remission that may inform a novel category of therapeutic targets.

引用

页码：13 / 23

页数：11

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