Fibroblast-like synoviocyte
| Fibroblast-like synoviocyte | |
|---|---|
| Details | |
| Location | Synovium |
| Anatomical terms of microanatomy] | |
Fibroblast-like synoviocytes (FLS) represent a specialised cell type located inside joints in the
Fibroblast-like synoviocytes in normal tissues
The inner lining of the joint consists of the synovium (also called the synovial membrane), a thin layer located between the joint capsule and the joint cavity. The word "synovium" is derived from the word "synovia" (or synovial fluid), which is a clear, viscous fluid produced by the synovium, and its main purpose is to reduce friction between the joint cartilages during movement. Synovium is also important to maintain proper joint function by providing the structural support and supply of the necessary nutrients to the surrounding cartilage. Synovial membrane is divided into two compartments – the outer layer (subintima) and the inner layer (intima). The inner layer is mainly composed of two cell types, specialized macrophages (macrophage-like synovial cells) and fibroblast-like synoviocytes, which are important in maintaining the internal joint homeostasis. These cells represent the main source of hyaluronic acid and also other glycoproteins, major components of the synovial fluid.[1][2]
Fibroblast-like synoviocytes are cells of
The role of fibroblast-like synoviocytes in the pathogenesis of rheumatoid arthritis
Synovial
FLS that are present in the synovium during RA display altered
The aggressive phenotype of FLS in RA and the effect these cells have on their microenvironment can be summarized into hallmarks that distinguish them from healthy FLS. These hallmark features of FLS in RA are divided into 7 cell-intrinsic hallmarks and 4 cell-extrinsic hallmarks.[5] The cell-intrinsic hallmarks are: reduced apoptosis, impaired contact inhibition, increased migratory invasive potential, changed epigenetic landscape, temporal and spatial heterogeneity, genomic instability and mutations, and reprogrammed cellular metabolism. The cell-extrinsic hallmarks of FLS in RA are: promotes osteoclastogenesis and bone erosion, contributes to cartilage degradation, induces synovial angiogenesis, and recruits and stimulates immune cells.[5]