Zebrafish have lubricated joints similar to ours and are a tractable model for arthritis research.

Soluble Fas ligand interacts specifically with tumor necrosis factor receptor superfamily (TNFRSF)10B, also known as death receptor 5, exacerbating arthritis in a Fas-independent manner.

Phosphorylation-mediated inactivation of pro-apoptotic BCL-2 family protein BAD confers the apoptosis resistance on synovial sublining macrophages, thereby contributing to the development of rheumatoid arthritis.

NFATc1 is identified as a molecular marker of articular cartilage progenitor cells and a transcriptional repressor of chondrocyte differentiation, providing fundamental insights into the origin and differentiation mechanism of articular chondrocytes.

A new role is identified for GLI1 in modulating the inflammatory response of macrophages and the overaction of osteoclasts in collagen-induced arthritis by collaboratively regulating DNMT1 and DNMT3a.

MiR 204/211 antagonize synovial inflammation and hyperproliferation by regulation of its downstream target gene Ssrp1, and decelerated RA progression.

Parathyroid hormone attenuates osteoarthritis pain and joint degeneration by modification of subchondral bone remodeling and could be a potential disease-modifying therapy for osteoarthritis.

Osteoarthritis pathogenesis is driven by IgE-mediated mast cell activation.

In localized autoimmune disease, there is autoantigen-driven expansion of both effector T cell and Treg clones that are highly persistent and are (re)circulating, and might represent interesting therapeutic targets.

Experimentation on patient biopsies, cell culture, and xenograft models demonstrates involvement of ErbB signaling and fibroblasts in lesion growth, implying that targeting of both stromal and endothelial cells could be a beneficial treatment strategy for patients with venous lesions.