Rheumatoid arthritis is an autoimmune disease that affects human cartilage and synovial tissue, due to the activation of T and B lymphocytes reactive to type II collagen present in the joints. It is thus a disease with characteristic of cellular and humoral immune response. Although there is not an experimental model that mimics all the features of human disease, the collagen-induced arthritis (CIA) in mice DBA/l is the main model for study of this disease. It has recently been shown that the CIA could also be induced in mice with different MHC haplotypes, such as that found in strain BALB/c, by administration collagen associated with exogenous proteins such as KLH (keyhole lympet hemocyanin) and OVA (ovalbumin). Manipulation of the immune system to the prophylaxis and treatment of autoimmunity has been studied in several laboratories. In this regard, promising results in preventing the installation of CIA in mice DBA/1 were obtained by oral administration of collagen before induction of disease. The oral tolerance is a special type of immune response of the digestive tract, leading to inhibition of systemic mechanisms of immunity that would normally be triggered by the administration of antigen by other means. The main cells involved in this process are the immature dendritic cells (DCs) and regulatory T cells (Tregs), which activity culminated in anergy or clonal deletion of activated T cells. It is a mechanism of negative regulation, and its understanding can yield therapies against a variety of chronic inflammatory autoimmune disorders, for example, rheumatoid arthritis. The main objective of this study is evaluate whether installation of CIA interferes with the induction of oral tolerance in mice of strain BALB/c. It is also purpose of this project to evaluate the possible modulation of the progression of arthritis induced by collagen + OVA in mice of the same lineage by adoptive transfer of dendritic cells obtained from mice tolerant to ovalbumin.
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