Rheumatoid arthritis (RA) is the most common inflammatory rheumatic disease. Destructive damage of the joints, resulting in physical disability, is the ultimate result of bone and cartilage damage mediated by the production of degradative enzymes and a wide array of inflammatory molecules. The etiopathogenesis of RA involves an intricate network of cell-cell interactions in the synovial tissue characterized by the proliferation of cells in the intimal lining of the joint, resulting in hyperplasia, pannus formation, and tissue inflammation and destruction. Fibroblast-like synoviocytes (FLSs) are mesenchymal derived cells responsible for providing support, nourishment and lubrication to the joint tissue. FLSs are one of the most prominent cells in inflamed tissue in RA. In the chronic inflammatory milieu of the rheumatoid synovium, these cells become autonomous, hyperplastic, and invasive and are the key source of inflammatory cytokines, chemokines, and matrix-degrading enzymes. No one-cell type exclusively account for the pathologic comportment of RA synovia. However, there is much yet to learn about the role of FLS in the aetiology, pathogenesis, and possible new therapeutical approaches to targeting these cells in RA.
The aetiology of RA is unknown and its pathogenesis is multifactorial and complex. It is believed that half of the risk of developing the disease is due to genetic factors. However, several environmental factors have been suggested as a "trigger" factor, which can be seen in the genome as epigenetic signatures that can favour an aggressive manifestation of the disease. Other components can also predispose the RA progression, such as changes in the synovia metabolism that can also be envisaged as a potential therapeutic strategy. Advances in knowledge of disease mechanisms in RA has led to the development of therapies effective for disease control. The benefit of using biological agents in RA, mediated by blocking cytokines or their receptor or acting on B cells and T lymphocytes, significantly altered the rheumatoid disease management. However, many more things need to be clarified regarding this important population of cells, the fibroblast-like synoviocytes (FLS), which can have positive or negative effects depending on the time, environment and evolution of the disease.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles covering, but not limited to, the following sub-topics:
• Normal synovial fibroblast characteristics and function
• Synovial fibroblast subsets and characteristics in RA
• Epigenomics of the synovial fibroblast in RA
• Metabolism of the RA synovial fibroblast
• Invasive behaviour of the RA synovial fibroblast
• Synovial fibroblast interactions with other synovial cells
• The synovial fibroblast and disease activity and severity in RA
Rheumatoid arthritis (RA) is the most common inflammatory rheumatic disease. Destructive damage of the joints, resulting in physical disability, is the ultimate result of bone and cartilage damage mediated by the production of degradative enzymes and a wide array of inflammatory molecules. The etiopathogenesis of RA involves an intricate network of cell-cell interactions in the synovial tissue characterized by the proliferation of cells in the intimal lining of the joint, resulting in hyperplasia, pannus formation, and tissue inflammation and destruction. Fibroblast-like synoviocytes (FLSs) are mesenchymal derived cells responsible for providing support, nourishment and lubrication to the joint tissue. FLSs are one of the most prominent cells in inflamed tissue in RA. In the chronic inflammatory milieu of the rheumatoid synovium, these cells become autonomous, hyperplastic, and invasive and are the key source of inflammatory cytokines, chemokines, and matrix-degrading enzymes. No one-cell type exclusively account for the pathologic comportment of RA synovia. However, there is much yet to learn about the role of FLS in the aetiology, pathogenesis, and possible new therapeutical approaches to targeting these cells in RA.
The aetiology of RA is unknown and its pathogenesis is multifactorial and complex. It is believed that half of the risk of developing the disease is due to genetic factors. However, several environmental factors have been suggested as a "trigger" factor, which can be seen in the genome as epigenetic signatures that can favour an aggressive manifestation of the disease. Other components can also predispose the RA progression, such as changes in the synovia metabolism that can also be envisaged as a potential therapeutic strategy. Advances in knowledge of disease mechanisms in RA has led to the development of therapies effective for disease control. The benefit of using biological agents in RA, mediated by blocking cytokines or their receptor or acting on B cells and T lymphocytes, significantly altered the rheumatoid disease management. However, many more things need to be clarified regarding this important population of cells, the fibroblast-like synoviocytes (FLS), which can have positive or negative effects depending on the time, environment and evolution of the disease.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles covering, but not limited to, the following sub-topics:
• Normal synovial fibroblast characteristics and function
• Synovial fibroblast subsets and characteristics in RA
• Epigenomics of the synovial fibroblast in RA
• Metabolism of the RA synovial fibroblast
• Invasive behaviour of the RA synovial fibroblast
• Synovial fibroblast interactions with other synovial cells
• The synovial fibroblast and disease activity and severity in RA
