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Arthritis Res. 2000;2(5):356-60. Epub 2000 Jun 23.

Fibroblast biology. Effector signals released by the synovial fibroblast in arthritis.

Author information

1
Clinical Immunology & Rheumatology Unit, University of Rochester Medical Center, Rochester, New York 14642, USA. christopher_ritchlin@urmc.rochester.edu

Abstract

There is mounting evidence indicating that the synovial fibroblast is a direct effector of tissue injury and matrix remodeling in inflammatory synovitis. Through the elaboration of effector signals including cytokines and chemokines, mesenchymal cells stimulate or suppress inflammation via autocrine and paracrine mechanisms. Synovial fibroblasts are the principal cells mediating joint destruction through secretion of metalloproteinases, and recent evidence suggests that they may also promote bone resorption by stimulating osteoclastogenesis. Moreover, they may play an integral role in the initial phases of synovitis by releasing chemokines that recruit leukocytes to the joint, and cytokines that trigger angiogenesis. Studies focusing on synoviocyte-leukocyte interactions mediated via the cytokine network and the role of cell-cell contact in driving synoviocyte activation will help define the complex interplay that leads to the initiation and perpetuation of synovial inflammation.

PMID:
11094448
PMCID:
PMC130136
DOI:
10.1186/ar112
[Indexed for MEDLINE]
Free PMC Article

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