The common genetic hypothesis of autoimmune/inflammatory disease

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Abstract
Individual inflammatory and autoimmune diseases are discrete clinical entities. The clinical presentation of any specific inflammatory disease is the culmination of complex interactions between genetics, primary and secondary immune effector mechanisms, and environmental triggers. Although often different in clinical presentation, common cellular and molecular immune pathways have been shown to be intimately involved in the destruction of different target tissues in different disease states, which ultimately defines specific diseases. At the genetic level, comparative genomic analysis of autoimmune and inflammatory disorders suggests shared genetic components for these clinically related diseases. This leads to a common genetic hypothesis which states that, unlike classical mendelian genetic disorders, common autoimmune and inflammatory disorders arise from combinatorial interactions of common non-disease specific loci, disease specific loci, and specific environmental triggers.

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