Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Jun 19:10:1395.
doi: 10.3389/fimmu.2019.01395. eCollection 2019.

Regulation of Immune Responses and Chronic Inflammation by Fibroblast-Like Synoviocytes

Affiliations
Review

Regulation of Immune Responses and Chronic Inflammation by Fibroblast-Like Synoviocytes

Hiroyuki Yoshitomi. Front Immunol. .

Abstract

Synovial tissue is a membranous non-immune organ lining joint cavities where it supports local immune responses, and functions directly and indirectly in joint destruction due to chronic inflammatory diseases such as rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLS), the dominant non-immune cells of synovial tissues, mainly contribute to joint destruction via multiple mechanisms. In RA, FLS respond to endogenous ligands of pattern recognition receptors (PRRs) and inflammatory cytokines as non-immune cells. In addition, FLS aid in the activation of immune responses by interacting with immune cells and by supporting ectopic lymphoid-like structure (ELS) formation in synovial tissues. Moreover, FLS directly cause the pathogenicity of RA i.e., joint deformities. Here, we describe new findings and review the mechanisms underlying the regulation of immune reactions by non-immune FLS and their roles in inflammatory diseases such as RA.

Keywords: autoantibodies; ectopic lymphoid-like structures (ELSs); fibroblast-like synoviocytes (FLSs); immune cells; non-immune cells; rheumatoid arthritis; synovial tissue.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic outline of interactions between FLS and immune cells.
Figure 2
Figure 2
Schematic outline of FLS contribution to TLO formation.

References

    1. Pitzalis C, Jones GW, Bombardieri M, Jones SA. Ectopic lymphoid-like structures in infection, cancer and autoimmunity. Nat Rev Immunol. (2014) 14:447–62. 10.1038/nri3700 - DOI - PubMed
    1. Schellekens GA, Visser H, de Jong BA, van den Hoogen FH, Hazes JM, Breedveld FC, et al. . The diagnostic properties of rheumatoid arthritis antibodies recognizing a cyclic citrullinated peptide. Arthritis Rheum. (2000) 43:155–63. 10.1002/1529-0131(200001)43:1<155::AID-ANR20>3.0.CO;2-3 - DOI - PubMed
    1. Bartok B, Firestein GS. Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis. Immunol Rev. (2010) 233:233–55. 10.1111/j.0105-2896.2009.00859.x - DOI - PMC - PubMed
    1. Ospelt C, Brentano F, Rengel Y, Stanczyk J, Kolling C, Tak PP, et al. . Overexpression of toll-like receptors 3 and 4 in synovial tissue from patients with early rheumatoid arthritis: toll-like receptor expression in early and longstanding arthritis. Arthritis Rheum. (2008) 58:3684–92. 10.1002/art.24140 - DOI - PubMed
    1. Brentano F, Schorr O, Gay RE, Gay S, Kyburz D. RNA released from necrotic synovial fluid cells activates rheumatoid arthritis synovial fibroblasts via Toll-like receptor 3. Arthritis Rheum. (2005) 52:2656–65. 10.1002/art.21273 - DOI - PubMed

Publication types

MeSH terms