Abstract
The antigens that trigger the pathogenic immune response in rheumatoid arthritis remain unknown. Until recently it was assumed that joint-specific antigens were the targets of arthritogenic T lymphocytes and B lymphocytes in rheumatoid arthritis. Consequently, murine models of arthritis are induced by immunization with either joint-specific antigens such as type II collagen or microbial products such as streptococcal cell wall. In the K/BxN T-cell receptor transgenic mouse model, arthritis is caused by a systemic autoimmune response to the ubiquitously expressed glycolytic enzyme glucose-6-phosphate isomerase (G6PI). More recently it was shown that G6PI immunization induces severe symmetrical peripheral polyarthritis in genetically unaltered DBA/I or SJL mice [1,2]. T cells are indispensable for both the induction and the effector phase of G6PI-induced arthritis. Arthritis is cured by depletion of CD4 cells. In contrast, antibodies and FcγR effector cells are necessary but not sufficient for G6PI-induced arthritis in genetically unaltered mice [1]. Both the induction and effector phase of arthritis induced by a systemic autoimmune response can be dissected and preventive and therapeutic strategies evaluated in this model.
Highlights
Rheumatoid arthritis is a chronic inflammatory disorder that primarily affects the joints and results in the destruction of cartilage and subchondral bone by the inflamed synovium
peripheral blood mononuclear cells (PBMC) from systemic sclerosis (SSc) patients responded to TNFα with significantly higher production of leukotriene E4 (LTE4) in comparison with healthy controls (P < 0.05 at 1 hour), while there were no significant differences in TNFα-induced production of 15-hydroxyeicosatetraenoic acid (15-HETE) between SSc patients and controls
It was shown that attachment of synovial fibroblasts (SF) that this association was completely dependent on concomitant from rheumatoid arthritis patients to laminin-111 (LM-111) induced carriage of the PSORS1 risk allele
Summary
Rheumatoid arthritis is a chronic inflammatory disorder that primarily affects the joints and results in the destruction of cartilage and subchondral bone by the inflamed synovium. A observed in affected joints of rheumatoid arthritis (RA) patients, as tourniquet was not used during the procedures and the skin portal well as extensive synovial infiltration of inflammatory cells. These conflicting observations suggest that the regulation of IL-7 expression is tightly controlled at the level of tissue specificity To support this hypothesis, we showed that several cytokines have a different effect on IL-7 production in BM StrC, epithelial cells from the liver and gut. TRU-015 is a CD20-directed small modular immunopharmaceutical drug candidate that effectively depletes B lymphocytes in cynomolgus monkeys in a dose-dependent manner, and improves survival in mouse xenograft tumor models [4,5].
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