T cell subsets and their role in the pathogenesis of rheumatic disease

被引:117
作者
Gizinski, Alison M. [1 ]
Fox, David A. [2 ]
机构
[1] Univ Arkansas, Little Rock, AR 72204 USA
[2] Univ Michigan, Ann Arbor, MI 48109 USA
关键词
biologic therapeutics; regulatory T cell; TH17; COLLAGEN-INDUCED ARTHRITIS; TH17; CELLS; AUTOIMMUNE ARTHRITIS; DOUBLE-BLIND; TREG CELLS; INTERLEUKIN-6; INHIBITION; EXPRESSION; BALANCE; ANTIGEN;
D O I
10.1097/BOR.0000000000000036
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Purpose of reviewT lymphocytes are critical to the pathogenesis of systemic rheumatic diseases. Understanding of the roles of T cells in disease has been enriched by the description of highly distinct effector subsets of CD4(+) T lymphocytes. The purpose of this review is to describe selected advances in the biology of T lymphocytes that are pertinent to the pathogenesis or treatment of rheumatic diseases.Recent findingsKnowledge is expanding about not only pathogenic effector T cell subsets, such as the T(H)17 cells, but also of regulatory T cells (T-reg), the functions of which are defective, but correctable, in several rheumatic diseases. Although the initial agent that demonstrated a role for T cells in rheumatoid arthritis was CTLA4-Ig (abatacept), use of this biologic is now expanding to other rheumatic diseases. Moreover, effects of other biologics are now understood to in part be mediated by effects on T cell subsets. Experimental model systems in rodents continue to be valuable testing grounds for future approaches to treatment of human disease. Meanwhile, the roles of effector T cell subsets are becoming clearer in conditions such as Sjogren's syndrome and scleroderma. Finally, rheumatic diseases, including rheumatoid arthritis and spondyloarthropathies, have been critical for identification of new innate-like T cell subsets.SummaryImbalances in the numbers and functions of specific T cell subsets are key pathogenic derangements in systemic rheumatic diseases, and these insights are leading to changes in clinical practice.
引用
收藏
页码:204 / 210
页数:7
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