Open AccessImmunomodulatory role of T helper cells in rheumatoid arthritis
Author(s) -
Pan Luo,
Peixu Wang,
Jiawen Xu,
Weikun Hou,
Peng Xu,
Ke Xu,
Lin Liu
Publication year - 2022
Publication title -
bone and joint research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.639
H-Index - 31
ISSN - 2046-3758
DOI - 10.1302/2046-3758.117.bjr-2021-0594.r1
Subject(s) - proinflammatory cytokine , immunology , chemokine , t cell , immune system , tumor necrosis factor alpha , ccl5 , cytotoxic t cell , cytokine , medicine , cancer research , biology , inflammation , il 2 receptor , biochemistry , in vitro
Rheumatoid arthritis (RA) is an autoimmune disease that involves T and B cells and their reciprocal immune interactions with proinflammatory cytokines. T cells, an essential part of the immune system, play an important role in RA. T helper 1 (Th1) cells induce interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin (IL)-2, which are proinflammatory cytokines, leading to cartilage destruction and bone erosion. Th2 cells primarily secrete IL-4, IL-5, and IL-13, which exert anti-inflammatory and anti-osteoclastogenic effects in inflammatory arthritis models. IL-22 secreted by Th17 cells promotes the proliferation of synovial fibroblasts through induction of the chemokine C-C chemokine ligand 2 (CCL2). T follicular helper (Tfh) cells produce IL-21, which is key for B cell stimulation by the C-X-C chemokine receptor 5 (CXCR5) and coexpression with programmed cell death-1 (PD-1) and/or inducible T cell costimulator (ICOS). PD-1 inhibits T cell proliferation and cytokine production. In addition, there are many immunomodulatory agents that promote or inhibit the immunomodulatory role of T helper cells in RA to alleviate disease progression. These findings help to elucidate the aetiology and treatment of RA and point us toward the next steps. Cite this article: Bone Joint Res 2022;11(7):426-438.