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Search for: [Abstract = "Rheumatoid arthritis \(RA\) an example of an autoimmune disease. While not uncommon, with a prevalence of 1% worldwide, the pathogenesis of RA is not clear yet. At present it is thought that the pathogenesis of RA is the result of an inflammatory response mediated by CD4\+ Th1 cells that recognize unidentified antigens that are present in joints. Following antigen\-induced activation, self\-specific Th1 cells release cytokines that initiate inflammatory processes in the joint. This leads to polimorphonuclear and macrophage accumulation and subsequent destruction of cartilage and erosion of bone with extra\-articular manifestations. Recently, there is a growing evidence for a role for Th17 lymphocytes in autoimmunity including RA and that this population of helper cells may be more important to the pathogenesis of RA than Th1 cells. Research on autoimmune disease pathogenesis, and development and of new drugs is possible thanks to animal models that mimic human diseases. Collagen\-induced arthritis \(CIA\) in genetically prone strains of mice, rats, rabbits or rhesus monkeys has been used as an experimental model of RA, as they share many histological and immunological characteristics. CIA can be induced by subcutaneous \(s.c.\) injection of collagen II in complete Freund’s adjuvant \(CFA\). There are many drugs that are used in therapy of autoimmune diseases including RA. It is noteworthy that, apart from drugs as gold salts, sulphasalazine, corticosteroids, there are medicines that interfere with immune processes. These include cyclosporine A, antibodies that neutralize TNF\-α or IL\-1R antagonists. However, most of these inhibit immune response non\-specifically and cause many side effects. For many years there have been numerous efforts to create a vaccine that can protect from autoimmune diseases including RA. One possible method relies on the induction of oral tolerance. In an animal model it was shown that feeding with collagen induced strong tolerance in the periphery, resulting in significantly reduced symptoms of CIA. Similar observations were also made in experimental autoimmune encephalomyelitis \(EAE\), another autoimmune disease mediated by Th1\/Th17 lymphocytes. However, clinical trials in humans showed no benefit in RA or multiple sclerosis patients fed with collagen or myelin basic protein, respectively. Although skin is considered to be an organ where immune responses are easily induced, little attention has been given to skin induced tolerance. Wang, et. al. showed that epicutaneous \(EC\) application of the protein antigen OVA resulted in allergic dermatitis accompanied by the appearance of IL\-4 secreting cells. In addition, Herrick, et al. showed that EC immunization with protein antigen induced a Th2\-mediated animal model of asthma. These data may suggest that, similar to mucosal exposure, EC immunization could induce peripheral tolerance when special conditions are fulfilled. Previous work carried out in the Department of Human Developmental Biology, Jagiellonian University College of Medicine both in CS and EAE models showed that EC immunization with protein antigen strongly suppressed the induction of the T cell mediated immune response. Further work employing allogeneic skin grafts showed that EC immunization with a protein antigen delays graft rejection. In the current study, It was investigated if EC immunization with a soluble protein antigen via a gauze skin patch could ameliorate the inflammatory response during CIA. It was shown that EC immunization with collagen II \(COLL II\) prior to induction of CIA reduced disease severity in susceptible DBA\/1 mice. The optimal dose of COLL II that inhibits CIA was found to be between 30 and 100 μg\/animal. The decrease in disease severity correlated with milder histological changes, reduced MPO activity in joint tissue, decreased production of pathogenic anti\-type II collagen IgG2a antibody and reduced level of anti\-cyclic citrulinated peptide \(anti CCP\) IgG antibodies."]

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