The role of inflammatory cytokines and NF-κB/MAPK signaling pathways in the evolution of familial Mediterranean fever: Current clinical perspectives and potential therapeutic approaches

Familial Mediterranean fever (FMF) is one of the social and health care problems for several populations that is known as a historically endemic disease of inflammatory nature. FMF, albeit a rare disorder, is characterized by recurrent fevers and painful inflammation of various body parts, especially the abdomen, lungs, and joints. FMF is typically characterized by inflammation of the abdominal lining (peritonitis), inflammation of the lining surrounding the lungs (pleurisy), painful, swollen joints (arthralgia and occasionally arthritis), and a characteristic ankle rash, a condition that is referred to as recurrent polyserositis, or familial paroxysmal polyserositis. Moreover, FMF is an inherited inflammatory disorder usually occurring in people of Mediterranean origin – including Sephardic Jews, Arabs, Armenians, and Turks; but it may ostensibly affect any other ethnic group, however, rarely. While there’s no cure for this disorder, FMF is typically diagnosed during childhood, and signs and symptoms are treatable – or even preventable – by specialized medical attrition. The inflammatory signaling pathways associated with the evolution of FMF are currently being unraveled has that has therapeutic repercussions. In this review, I recap major concepts associated with the cellular and molecular immunology of FMF, especially shedding light on the likely roles of inflammatory cytokines, the transcription factor nuclear factor (NF)-κB, and the superfamily of mitogen-activated protein kinases (MAPKs). Furthermore, I summarize current advances for the clinical treatments available for FMF.