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Alexandre Alcaïs^a,b,c, Claire Fieschi^a,b,c, Laurent Abel^a,b,c, and Jean-Laurent Casanova^a,b,c

^a A.A., C.F., L.A., and J.-L.C. are at Laboratory of Human Genetics of Infectious Diseases, University of Paris René Descartes-INSERM U550, Necker Medical School, 75015 Paris, France, EU.
^b C.F. is at Adult Immunopathology Unit, Saint Louis Hospital, 75010 Paris, France, EU.
^c J.-L.C. is at Pediatric Hematology-Immunology Unit, Necker Hospital, 75015 Paris, France, EU.

CORRESPONDENCE J.-L.C.: casanova{at}necker.fr

Abstract
Disseminated disease in children and pulmonary disease in adults constitute two major epidemiological and clinical forms of tuberculosis. Paradoxically, only a small fraction of infected individuals develop clinical tuberculosis, typically one form of the disease or the other. Mendelian and complex genetic predispositions to tuberculosis were reported recently in children and adults, respectively. Here, we argue that tuberculosis and its clinical expression largely reflect the underlying human genetic background.

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