About this Research Topic
Rheumatoid Arthritis (RA) is a common rheumatic disorder characterized by persistent synovial inflammation and destruction of joints. Fibroblast-like Synoviocytes (FLSs), the cells unique to the synovial intimal lining, are a prominent component of hyperplastic synovial pannus tissue that mediates cartilage and bone damage. RA FLSs display important immunomodulatory functions through secretion of inflammation mediators and through direct interactions with several synovial-infiltrated immune cells including macrophages, B-cells and T-cells. Moreover, RA FLSs also exhibit surprisingly aggressive behavior, such as resistance to apoptosis, anchorage-independent growth, increased migration, and the ability to invade; this last trait is why these cells are also known as “imprinted aggressors”. Increasing evidence indicates that modulating activated-FLS aggression may be a new therapeutic strategy for reducing joint damage in RA.
In this Research Topic, we focus on discussing the mechanisms by which FLSs mediate inflammation and act as imprinted aggressors in the progression of RA. We welcome the submission of Original Research Articles as well as Reviews that cover, but are not limited to, the following topics:
1. Recent findings on the FLS-mediated immunopathology in RA
2. Interaction of FLS with other synovial immune cells such as macrophages, T-cells, B-cells and dendritic cells in RA
3. The role of protein post-translational modifications (PTMs), including phosphorylation, glycosylation, SUMOylation, nitrosylation, methylation, acetylation, lipidation and proteolysis in regulating FLS-mediated inflammation
4. Role of epigenetic alterations, such as DNA methylation, histone methylation, histone acetylation, and expression of microRNAs (miRNAs) and long noncoding RNA (lncRNA), in controlling the function of RA FLSs and immune cells involved in RA.
5. The role of metabolic changes and mitochondrial homeostasis in modulating RA FLS- or rheumatoid-associated immune cell-mediated synovial inflammation.
6. Contribution of abnormal cytosolic nucleic acid-sensing pathways to dysfunction of RA FLSs and immune cells involved in RA.
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