The immunopathogenesis of fibrosis in systemic sclerosis

被引：147
作者：
Brown, M. [1 ]
O'Reilly, S. [1 ]
机构：
[1] Northumbria Univ, Fac Hlth & Life Sci, Ellison Pl, Newcastle Upon Tyne NE2 8ST, Tyne & Wear, England
来源：
CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2019年 / 195卷 / 03期
关键词：
arthritis (including rheumatoid arthritis); B cells; T cells; Toll-like receptors (TLRs); GROWTH-FACTOR-BETA; TUMOR-NECROSIS-FACTOR; REGULATORY B-CELLS; MONOCYTE CHEMOATTRACTANT PROTEIN-1; BLOOD MONONUCLEAR-CELLS; T-CELLS; DENDRITIC CELLS; DERMAL FIBROBLASTS; PERIPHERAL-BLOOD; TOPOISOMERASE-I;
D O I：
10.1111/cei.13238
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Systemic sclerosis (SSc) is an idiopathic systemic autoimmune disease. It is characterized by a triad of hallmarks: immune dysfunction, fibrosis and vasculopathy. Immune dysfunction in SSc is characterized by the activation and recruitment of immune cells and the production of autoantibodies and cytokines. How immune abnormalities link the fibrosis and vasculopathy in SSc is poorly understood. A plethora of immune cell types are implicated in the immunopathogenesis of SSc, including T cells, B cells, dendritic cells, mast cells and macrophages. How these different cell types interact to contribute to SSc is complicated, and can involve cell-to-cell interactions and communication via cytokines, including transforming growth factor (TGF)-beta, interleukin (IL)-6 and IL-4. We will attempt to review significant and recent research demonstrating the importance of immune cell regulation in the immunopathogenesis of SSc with a particular focus on fibrosis.
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收藏
页码：310 / 321
页数：12
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