Irisin mitigates rheumatoid arthritis by suppressing mitochondrial fission via inhibiting YAP-Drp1 signaling pathway.

Background: Irisin is a hormone-like factor secreted by muscle cells and produced by cleavage of the membrane protein fibronectin type III domain protein 5 (FNDC5), which exerts anti-inflammatory and anti-proliferative effects. However, the effects and the underlying mechanisms of irisin in rheumatoid arthritis (RA) are still unclear.

Method: Collagen-induced arthritis (CIA) model was induced in DBA/1 mice and then treated with irisin.

Monocytes in rheumatoid arthritis: Circulating precursors of macrophages and osteoclasts and, their heterogeneity and plasticity role in RA pathogenesis.

Rheumatoid arthritis (RA) is a chronic systemic, autoimmune and inflammatory disease represented as synovitis, pannus formation, adjacent bone erosions, and joint destruction. The major cells involved in the perpetuation of RA pathogenesis are CD4 T-cells (mainly Th1 cells and Th17 cells), fibroblasts like synoviocytes (FLS), macrophages and B cells. Other autoimmune cells such as dendritic cells, neutrophils, mast cells, and monocytes also contribute to RA pathogenesis.

Activation of the bile acid receptor GPBAR1 (TGR5) ameliorates interleukin-1β (IL-1β)- induced chondrocytes senescence.

Osteoarthritis is the most common chronic condition of the joint disease. Chondrocyte is the sole cell type in joint tissues. Senescence of chondrocytes is known to contribute to the causation of osteoarthritis.

A Single Microorganism Epitope Attenuates the Development of Murine Autoimmune Arthritis: Regulation of Dendritic Cells the Mannose Receptor.

A single epitope of analog of the receptors for activated C kinase (LACK) from , the polypeptide LACK, is recognized by Vβ4/Vα8 T cells, and activate these cells that drives the subsequent T helper (Th)2 response. This study was undertaken to investigate the therapeutic potential of the LACK epitope in murine autoimmune arthritis models. To explore the influence of the LACK epitope on murine collagen antibody-induced arthritis, as well as its immunological mechanism, we vaccinated or treated mice with a LACK epitope expression plasmid or polypeptide.

Inhibition of microRNA-34a ameliorates murine collagen-induced arthritis.

Rheumatoid arthritis (RA) is one of the most frequently occurring autoimmne diseases, with symptoms including synovium hyperplasia, immune disorder, cartilage damage and bone resorption. It has previously been demonstrated that microRNA-34a (miR-34a) may participate in cell apoptosis, immune activation and bone metabolism, therefore the present study investigated the effects of miR-34a on RA. Collagen-induced arthritic (CIA) mice were employed as a murine model of experimental arthritis, and it was demonstrated that the level of miR-34a in the spleens, lymph nodes and synovium was increased in the CIA mice compared with normal DBA/1j mice.

Neuropsychiatric involvement in lupus is associated with the Nogo-a/NgR1 pathway.

Neuroinflammation- and neurodegeneration-induced nerve injury may represent important components of neuropsychiatric lupus (NPSLE). Myelin-associated neurite outgrowth inhibitor (Nogo)-a and its receptor, NgR1, limit recovery of the adult central nervous system after injury. We detected a soluble Nogo-a product in the cerebral spinal fluid of patients with NPSLE.

Intra-Articular Injection of Human Synovial Membrane-Derived Mesenchymal Stem Cells in Murine Collagen-Induced Arthritis: Assessment of Immunomodulatory Capacity In Vivo.

The aim of this study was to evaluate the efficacy of human synovial membrane-derived MSCs (SM-MSCs) in murine collagen-induced arthritis (CIA). Male mice (age 7-9 weeks) were injected intra-articularly with SM-MSCs obtained from patients with osteoarthritis, on days 28, 32, and 38 after bovine type II collagen immunization. The efficacy of SM-MSCs in CIA was evaluated clinically and histologically.