The immune system has highly evolved structured mechanisms to efficiently combat infections and cancers. However, its inbuilt complexicity creates a potential for causing diseases if not tightly regulated. Thus, autoimmune diseases could result from defects in the regulation of immune pathways resulting in the immune systems inability to distinguish self from non-self antigens (Ags), or the inability to suppress emerging autoreactive clones. This leads to immune responses to unlimited supplies of autoAgs, chronic inflammation and damage to tissues. Attempts to dissect the pathogenesis have shown that defects in T- and B-lymphocytes, innate immune cells and the complement system could trigger autoimmunity. Further, the level of involvement of different elements is varying in different diseases, and even within clinical subsets in the genetically diverse human population. The development of appropriate therapies has also been hampered by the need to delineate which mechanisms triggers a given disease and which ones sustain this same condition has been difficult because of the multiplicity of predisposing factors, susceptibility genes, and etiologies. A strategy to treat immune-mediated diseases in the clinic was initiated when the most evident abnormalities were targeted with inhibiting monoclonal antibodies or soluble receptors. Thus, tumor-necrosis factor α inhibitors were used for treating patients with rheumatoid arthritis and Crohns diseases. The strategy proved to be successful, so that hundreds of thousand of patients are currently treated with these agents.
Keywords: Autoimmune Diseases, tumor-necrosis factor α inhibitors, cancers, rheumatoid arthritis, immune system, Pathophysiology, chronic inflammation, Crohn's diseases
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