Crosstalk between synovial macrophages
and fibroblasts in rheumatoid arthritis
Noritaka Saeki1,2 and Yuuki Imai2,3
1Division of Medical Research Support, Advanced Research Support Center, 2Division of Integrative Pathophysiology, Proteo-Science Center and 3Department of Pathophysiology, Graduate School of Medicine, Ehime University, Ehime, Japan
Corresponding Author: Noritaka Saeki or Yuuki Imai, Ehime University, Shitsukawa, Toon, Ehime, 791-0295 Japan. e-mail: nsaeki@m.ehime-u.ac.jp or y-imai@m.ehime-u.ac.jp
Summary. Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammation of joints. Abnormally activated cells such as synovial macrophages and synovial fibroblasts induce RA pathogenesis and ultimately joint destruction. Since macrophages can change their own characteristics depending on the microenvironmental condition, it has been suggested that activation and remission of RA are regulated by crosstalk between synovial macrophages and other cells. Moreover, recent findings of hetero-geneity of synovial macrophages and fibroblasts support the idea that complex interactions regulate RA from its onset to remission. Importantly, an understanding of the intercellular crosstalk in RA is far from complete. Here, we summarize the molecular mechanisms underlying the pathological development of RA with particular reference to the crosstalk between synovial macrophages and fibroblasts. Histol Histopathol 38, 1231-1238 (2023)
Key words: Rheumatoid arthritis, Crosstalk, Synovial macrophages, Synovial fibroblasts
DOI: 10.14670/HH-18-628
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ŠThe Author(s) 2023. Open Access. This article is licensed under a Creative Commons CC-BY International License. |
