Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. It affects the peripheral joints and is characterized by a chronic progressive inflammatory destruction of cartilage and subchondral bone, leading to erosive joint destruction and deformities. Cellular and humoral reactions occurring in the synovial tissue and in the joint space produce mediators attracting inflammatory cells and causing cartilage degradation. Traditionally this disease is treated by medicals with antiinflammation effects.

The articular cartilage is an important component of human organism that has elasticity and lowfriction surface. The structure consist of collagens and proteoglicans. The structural elements of the cartilage are typical to that tissue and could, in part, account for the localization of the inflammatory response to the joint. For this reason cartilage is of particular interest in autoimmunity as it may represent a source of antigens. The antibodies to type II collagen demonstrable in the blood, cartilage and synovium. The levels of these antibodies in synovial fluid are significantly higher in RA than in patients affected with other arthritides leading into a noticeable mononuclear cell proliferation. This prevalence suggest an intra–articular antigen–driven immune process.

Sensitization with collagens can produce autoimmune rheumatic diseases in experimental models. The mechanisms determining the trigger of a cartilage–specific immune response, its development and outcome are poorly understood.

Although the models of arthritis are not an exact reflection of the situation in RA, they are widely used to investigate the pathogenesis of RA and its treatment possibilities. All models of arthritis in animals have different characteristics, and the knowledge from all of these models can be used to stady most aspects of RA, The most common model of arthritis is induced in rats by immunization with native collagen II emulsified in Freund’s adjuvant and called CIA. CIA is characterized by similar pathophysiological and pathobiochemical changes as RA in humans. It is an immunologically complex model involving both cellular and humoral mechanisms and has been used for many years for the evaluation of antirheumatic agents. The pathogenic mechanism of chronic inflammation is associated with an increased production autoantibodies, cytokines and activation of immune cells. It is an extensively studies form of experimental arthritis aimed to provide careful information on the nature of autoreactivity. CIA is the example of immunological mediated damage of joints. CIA is usefull model for studing the involving of cytokines and other biological agents in pathogenesis of damaged joints. The modern alternative method of treatment is the influences on the immunologic factors, which increased during acute stage of disease and become not active during remission.

In conclusion, the results demonstrated that the light course of CIA are associated with antibodies to collagen II, and the severest course of arthritis and pathomorphological changes in joints were revealed in rats with the presence of antibodies to cartilage oligomeric matrix protein and activated T-lymphocytes – chelper type 17. On the ground of data of literature we can make a conclusion, that the using of model of CIA is more usefull for the modelling of the early stage of RA in humen.

Keywords: rheumatiodal arthritis, mechanisms of immunopathology, collagen–induced arthritis, rats

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