In the course of autoimmune diseases, the immune system, upon reacting to bacteria, viruses, and other exogenous pathogens, also can attack self-antigens and tissues. Numerous autoimmune diseases are known, each of them exhibiting a distinct general etiopathology and affecting a limited number of defined self-antigens and tissues. Some autoimmune diseases are clinically heterogeneous and merely defined by common clinical criteria. These diseases may resemble a collection of genuinely distinct autoimmune disorders that share only distinct features. Examples include such widespread autoimmune disorders as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Frequently, these diseases initially present with mild symptoms but then become chronic and progressive, eventually resulting in severe and irreversible obstructions.
Autoimmune diseases affecting humans and animals are genetically complex [1,2]. Multiple gene defects contributing to the development of lupus in the NZB/W mouse model and the development of pristane-induced arthritis in particular rat strains have been identified [3-5]. Due to the complexity of factors influencing autoimmunity, the pathomechanisms of autoimmune diseases are diverse. Often, effector mechanisms of the innate immune system as well as of the adapted immune system are involved [6-10]. Autoreactive B cells, autoantibodies, and autoreactive effector T cells targeting specific self-antigens mediate the tissue specificity observed for particular autoimmune diseases. Complement, macrophages, and a self-sustaining chronic inflamma tory environment substantially contribute to the local pathogenesis [11-13]. Though in some animal models either autoreactive B cells or autoreactive T cells alone can be sufficient to induce an autoimmune disease, usually several mechanisms and cell types contribute to the development and/or maintenance of immunopathology in a cooperative manner [5, 14-16]. However, the factors initiating an autoimmune disease or promoting acute autoreac-tivity could be different from those driving the chronic course of that very same disease . Here, we will discuss pathological mechanisms involved in autoimmune diseases and their contribution to maintaining a chronic course of disease, with a special focus on the role of the immunological memory in that process.
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