[21] Nonetheless, of particular interest in regards to autoimmune diseases, is evidence for the contribution of the microbiome to the development of Th17 T helper beta-catenin assay cells.[22] These cells are shown to be important for the pathogenesis of several autoimmune diseases[23] and the induction of these cells is dependent upon the microbiome. That immune system development depends on the microbiome has been amply demonstrated by germ-free conditions. Germ-free

individuals show reduced peripheral CD4+ T cells, reduced immunoglobulin levels, immune deviation toward a Th2 phenotype, among other defects. A paper in Cell by Ivanov and colleagues showed that mono-association of segmented filamentous bacteria with germ-free animals was sufficient to induce fully functional Th17 T helper cells.[6] These provocative data suggest that manipulation click here of the microbiome to alter the immune phenotype might be possible. Another recent paper shows that this same bacteria can drive experimental autoimmune disease.[24] Under germ-free conditions the K/BxN mouse, which under specific pathogen-free conditions develops inflammatory arthritis, has greatly attenuated disease. Mono-association with segmented

filamentous bacteria restores gut-associated Th17 cells, autoantibody production and arthritis in this arthritis model.[24] Other animal models of autoimmunity also depend on gut-derived Th17 cells.[25] Investigation of the role of a particular member of the mouth microbiome, namely, P. gingivalis, in the

pathogenesis of rheumatoid arthritis has been ongoing for several years. The accumulated data demonstrate a strong association Etomidate as well as a plausible biological mechanism. Involvement of the microbiome in other rheumatic diseases has not been extensively studied. However, gut-associated organisms are critical to the development and activation of the immune system, especially with regard to cell types intimately associated with autoimmunity. These data indicate that the relationship of the microbiome to autoimmune rheumatic disease is an area of high interest. “
“Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by periods of flares and remission, resulting in organ damage over time caused by persistent disease activity and treatment-related complications. Conventional therapies are not ideal in terms of efficacy and safety. Novel biological therapies are being developed to enhance therapeutic efficacy, minimize disease exacerbation and reduce toxicities. As dysregulation of B cells is the hallmark of SLE, B-cell targeted therapies are the focus of recent clinical research. Rituximab, a chimeric anti-CD20 monoclonal antibody, has been used with success in recalcitrant lupus manifestations. However, randomized controlled trials have failed to reveal its benefit in renal and non-renal SLE when combined with conventional immunosuppressive protocols.