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• W2397001436 abstract "The monogenic autoinflammatory diseases (AIDs) are characterized by episodic or persistent, seemingly unprovoked inflammation. They are caused by abnormal activation of the cells that mediate innate immunity, resulting from dysregulation of the physiological alarm responses to foreign or endogenous danger signals. Many of the affected genes that have been initially reported are directly or indirectly involved in the regulation of the Interleukin-1 (IL-1) cytokine signaling pathway in AID. Typically, there is no evidence of high-titer autoantibodies or antigen-specific T lymphocytes. However, some recently reported AIDs enlarge the autoinflammation spectrum by having features of immunodeficiency and autoimmunity, and by implicating other cytokines than IL-1, such as interferon α. Molecular insights have provided the basis for therapeutic interventions, comprising mostly IL-1 inhibitors.The concept of AID was introduced in the late 1990s, when the genetic causes of familial Mediterranean fever and the TNF receptor-associated periodic syndrome were identified. The monogenic AIDs are characterized by episodic or persistent, seemingly unprovoked inflammation. They are caused by abnormal activation of the cells that mediate innate immunity, resulting from dysregulation of the physiological alarm responses to foreign or endogenous danger signals. Many of the affected genes that have been initially reported are directly or indirectly involved in the regulation of the IL-1 cytokine signaling pathway in AID. Typically, there is no evidence of high-titer autoantibodies or antigen-specific T lymphocytes. However, some recently reported AIDs enlarge the autoinflammation spectrum by having features of immunodeficiency and autoimmunity, and by implicating other cytokines than IL-1, such as interferon α. This article will review the monogenic AIDs known up to 2014." @default.
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• W2397001436 date "2016-01-01" @default.
• W2397001436 modified "2023-09-29" @default.
• W2397001436 title "Monogenic Autoinflammatory Diseases" @default.
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• W2397001436 doi "https://doi.org/10.1016/b978-0-12-374279-7.18023-3" @default.
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