02045nas a2200277 4500000000100000008004100001260001300042653002600055653001800081653002000099653003800119653003400157653001100191653001700202653001200219653002500231100001800256700001200274700001400286245006600300300001000366490000700376050002100383520134900404022001401753 2013 d c2013 Jun10aCommunicable Diseases10aCrohn Disease10aGenetic Markers10aGenetic Predisposition to Disease10aGenome-Wide Association Study10aHumans10aInflammation10aleprosy10aMycobacterium leprae1 aGaschignard J1 aScurr E1 aAlcaïs A00a[Leprosy, a pillar of human genetics of infectious diseases]. a120-80 v61 aGASCHIGNARD 20143 a

Despite a natural reservoir of Mycobacterium leprae limited to humans and free availability of an effective antibiotic treatment, more than 200,000 people develop leprosy each year. This disease remains a major cause of disability and social stigma worldwide. The cause of this constant incidence is currently unknown and indicates that important aspects of the complex relationship between the pathogen and its human host remain to be discovered. An important contribution of host genetics to susceptibility to leprosy has long been suggested to account for the considerable variability between individuals sustainably exposed to M. leprae. Given the inability to cultivate M. leprae in vitro and in the absence of relevant animal model, genetic epidemiology is the main strategy used to identify the genes and, consequently, the immunological pathways involved in protective immunity to M. leprae. Recent genome-wide studies have identified new pathophysiological pathways which importance is only beginning to be understood. In addition, the prism of human genetics placed leprosy at the crossroads of other common diseases such as Crohn's disease, asthma or myocardial infarction. Therefore, novel lights on the pathogenesis of many common diseases could eventually emerge from the detailed understanding of a disease of the shadows.

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