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• W2040761623 abstract "Continuing to improve our management of patients with autoimmune disease remains one of many substantially unmet challenges confronting modern medicine. At its heart, this effort relies heavily on accessing an ever-expanding knowledge of normal immunology and the molecular and cellular basis of disease. Integrating the evolving concepts rooted in emerging technology at the bench and bringing these to the field of clinical autoimmunity must be thoughtfully coupled with the diverse needs of our patients. Yet in many instances we encounter difficulty in categorizing our patients, describing them with precision to our colleagues or predicting their response to therapy. Despite these severe limitations, great advances in therapy have taken place over the last decade. Clearly, we must gain greater understanding of the basic disease mechanisms in play before we can create more effective and safer therapies. Let me begin this editorial with a brief review of what pieces of this complex puzzle we currently seem to understand. Adaptive immune responses usually protect us against infection. These are thought to be initiated by antigen-specific T cells. Sometimes they occur instead against noninfectious agents and may be directed against self-antigens, resulting in serious, potentially catastrophic consequences. Why reactivity to self, which undoubtedly occurs with great frequency in states of health, should begin to pose problems remains uncertain. A number of mechanisms for dampening this process and rendering it clinically silent have been identified. These include T-cell editing, clonal anergy, which effectively precludes activation, and clonal deletion [1–4]. Human autoimmune diseases comprise a group of maladies arising from the loss of normal tolerance. When adaptive immune responses occur against infectious agents, the immune system attempts to clear the foreign antigen. When the identical reaction occurs against a self-antigen, complete clearance is usually impossible and the immune response culminates in the activation of effector-cell pathways and chronic inflammation. Thus, a perfectly good, normally protective process is corrupted and causes harm by virtue of its exaggerated amplitude and duration. The incidence of common autoimmune diseases, such as rheumatoid arthritis, Type 1 diabetes mellitus and Graves’ disease, appears to aggregate in certain families, suggesting genetically related susceptibility to multiple diseases. In fact, individuals and families manifesting one of these diseases have a substantially greater risk of developing another. Thus, a common genetic basis for multiple autoimmune diseases seems very likely and is currently supported by substantial evidence. The contribution of genetics to many of these diseases is probably relatively modest in some and more substantial in others. This insight is derived from identical twin studies [5,6]. It is thought to be in the 10–30% range. Thus, the environment must be considered as an important contributor to autoimmune disease susceptibility. Shared immunological mechanisms linking several diseases were proposed more than 40 years ago for autoimmune thyroid disease, Type 1 diabetes mellitus, systemic sclerosis and Sjogren’s syndrome [7,8]." @default.
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• W2040761623 date "2007-08-01" @default.
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• W2040761623 title "Is a common therapy for autoimmune disease possible?" @default.
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• W2040761623 doi "https://doi.org/10.2217/17460816.2.4.333" @default.
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