Recently, a regimen consisting

of rituximab and mycophenolate mofetil without oral corticosteroids was reported to be effective in lupus nephritis. While the efficacy of this regimen has to be confirmed, future controlled trials should focus on the efficacy of rituximab in refractory lupus manifestations and its synergistic effect with other immunosuppressive agents such as cyclophosphamide. In short-term randomized controlled trials, a non-significant increase in serious adverse events was observed in SLE patients treated with rituximab. Long-term safety data of rituximab in SLE, in particular the incidence of hypogammaglobulinemia and serious/opportunistic infections, have to be continuously surveyed. “
“Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by the sequestration of various Mitomycin C order leukocyte subpopulations within both the developing pannus and synovial space. The chronic nature of this disease results in inflammation of multiple joints, with subsequent destruction of the joint cartilage and erosion of bone. Identification

of selleck T helper (Th)17 cells led to breaking the dichotomy of the Th1/Th2 axis in immunopathogenesis of autoimmune diseases such as RA, and its experimental model, collagen-induced arthritis (CIA). Th17 cells produce cytokines, including interleukin (IL)-17, IL-6, IL-21, IL-22 and tumor necrosis factor

(TNF)-α, with pro-inflammatory effects, which appear to have a role in immunopathogenesis of RA. Regarding the wide ranging production of pro-inflammatory cytokines and chemokines by Th17 cells, it is expected that Th17 cell could be a potent pathogenic Mirabegron factor in disease immunopathophysiology. Thus the identification of effector mechanisms used by Th17 cells in induction of disease lesions may open new prospects for designing a new therapeutic strategy for treatment of RA. The newly identified CD4+ T helper (Th) cell subtype, Th17 cells, are characterized by production of a distinct profile of effector cytokines, including interleukin (IL)-17A, IL-17F, IL-6, IL-9, IL-21, IL-22, IL-26 and tumor necrosis factor (TNF)-α. They have probably evolved to promote host clearance of a range of pathogens distinct from those targeted by Th1 and Th2.[1, 2] Th17 produces cytokine profiles, including IL-17, IL-6, IL-21, IL-22 and TNF-α, which have pro-inflammatory functions, suggesting an important factor in immunopathogenesis of rheumatoid arthritis (RA), because the main feature of RA pathophysiology is the inflammatory reaction.[3-5] The first sign of Th17 cells identification relates to the role of these cells in host immune response to Borrelia burgdorferi which induced the production of IL-17 by Th17.