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Pubmed ID :12687139
Publication Date : //

Autoimmune Diseases: Problems of Pathogenesis, Diagnostics and Treatment.


Autoimmune diseases (AID) are pathological states wherein a disturbance of the regulation of physiological autoimmune processes results in the appearance of antibodies, T lymphocytes, specific in respect to components of self tissues, causing structural and/or functional disturbances in target organs. Studies conducted in respect of the pathogenesis of AID deal with its main components: 1) mechanisms of oligo-polyclonal B-cellular activation; 2) participation of autoantibodies, immune complexes, DTH effectors in the development of autoimmune inflammation; 3) participation of cytotoxic lymphocytes in the realization of inflammation; 4) participation of cytokines and growth factors in AID development; 5) the role of endothelial cells and adhesion molecules in the formation of inflammation during AID; 6) mechanisms of sclerogenesis; 7) the role of macrophages, neutrophils, platelets in the development of AID; 8) mechanisms for self-support of the autoimmune process; 9) the role of disturbances in apoptosis mechanisms. An important role in the realization of inflammation during autoimmune reactions belongs to various mediators of inflammation: prostaglandins, activated oxygen forms, proteinases and their inhibitors, vasoactive amines, nitrogen oxides, components of the complement system, and kinins. Early diagnosis of AID and improvements in the scheme of pharmacotherapy have made it possible to achieve substantial successes in treatment. The prospects of increasing the effectiveness of therapy is linked to the appearance of a new generation of preparations, developed on the base of profound knowledge of immunopathogenesis of organ specific and organ non-specific AID: the use of "anti-inflammatory cytokines", soluble cytokine receptors, antagonists of cytokine receptors, monoclonal antibodies to cytokines and membrane antigens of lymphocytes, inducers of apoptosis and others.

Authors : Shirinskiy Valery S. ,

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