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Review
. 2017 Oct 15;3(2):e000471.
doi: 10.1136/rmdopen-2017-000471. eCollection 2017.

Synovial fibroblasts in 2017

Caroline Ospelt  1
Affiliations
Review

Synovial fibroblasts in 2017

Caroline Ospelt. RMD Open. .

Abstract

Stromal cells like synovial fibroblasts gained great interest over the years, since it has become clear that they strongly influence their environment and neighbouring cells. The current review describes the role of synovial fibroblasts as cells of the innate immune system and expands on their involvement in inflammation and cartilage destruction in rheumatoid arthritis (RA). Furthermore, epigenetic changes in RA synovial fibroblasts and studies that focused on the identification of different subsets of synovial fibroblasts are discussed.

Keywords: fibroblasts; inflammation; rheumatoidarthritis.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Osteoarthritis (A) and rheumatoid arthritis (RA) synovium (B). Synovial fibroblasts are found in the lining as well as in the sublining layer of the synovium. Thickening of the lining layer, lymphocytic infiltration and increased formation of blood vessels can be seen in RA synovium.
Figure 2
Figure 2
Overview of key interactions between T cells and synovial fibroblasts. ALCAM, activated leukocyte cell adhesion molecule; CD40L, CD40 ligand; ICAM-1, intercellular adhesion molecule 1; LFA, lymphocyte function-associated antigen; MHC II, major histocompatibility complex II; TNFR1/2, tumour necrosis factor receptor 1/2; VCAM-1, vascular cell adhesion protein 1; VLA-4, very late antigen-4.
Figure 3
Figure 3
Attachment of rheumatoid arthritis (RA) synovial fibroblasts to cartilage and cartilage destruction. Impairment of cartilage structure and loss of proteoglycan were described as initiating events in the attachment of synovial fibroblasts to cartilage. Increased expression of α5β1 and its co-receptor syndecan 4 in RA synovial fibroblasts promotes binding of fibronectin, which can be deposited or exposed in damaged cartilage. High levels of proinflammatory factors such as tumour necrosis factor (TNF), interleukin (IL) 1 and toll-like receptor (TLR) ligands stimulate synovial fibroblasts to produce matrix-degrading molecules such as matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and cathepsins.
See this image and copyright information in PMC

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