This is the 18th year of ongoing research in 'autoinflammation'. Since the genetic and pathogenic characterization of the first autoinflammatory diseases—familial Mediterranean fever (FMF) and TNF-receptor associated periodic syndrome (TRAPS)—further genetic and clinical discoveries have advanced hand in hand with basic discoveries of innate-immune sensors and pathways that link danger-sensing to the production and release of key pro-inflammatory cytokines (1).
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