Inflammation in the spotlight—clinical relevance of genetic variants affecting nuclear factor κB and tumor necrosis factor receptor 1

Increased basal and chronic low-level activation of inflammation in patients with autoimmune disease has prompted many research lines trying to unravel the genetic control of the inflammatory cascades, being located at the forefront of such physiological disturbances. Accordingly, several abnormalities have been identified in cytokine-signaling pathways and immune receptors conducting the inflammatory response that commonly characterizes autoimmune reaction. Among the molecules involved in this kind of pathologies we identify Jak/Stat (1), Jun/Fos, p38, ERK1/3, and many others serine/threonine kinases involved in the MAP kinase transduction signal (2), and the NFκB (3).