02036nas a2200325   4500000000100000008004100001260001300042653001200055653003400067653002700101653002200128653002000150653001100170653001900181653001800200653001200218653000900230653002500239653002500264653003100289653001300320653001700333100001200350245011400362856004100476300001100517490000700528520116100535022001401696       1981                            d  c1981 Dec10aAnimals10aContinental Population Groups10aDisease Susceptibility10aDiseases in Twins10aGenetic Markers10aHumans10aImmunogenetics10aLeishmaniasis10aleprosy10aMice10aMice, Inbred Strains10aMycobacterium leprae10aMycobacterium tuberculosis10aPedigree10aTuberculosis1 aFine PE00aImmunogenetics of susceptibility to leprosy, tuberculosis, and leishmaniasis. An epidemiological perspective.  uhttp://ila.ilsl.br/pdfs/v49n4a09.pdf  a437-540 v493 a<p>The literature on the genetic regulation of susceptibility in leprosy, tuberculosis, amd leishmaniasis is critically reviewed. Of the three groups of diseases, leprosy has received the most attention from the standpoint of human genetics. There is now evidence that genetic factors, some of them HLA-linked, play a role in tuberculoid leprosy. However, the evidence leaves considerable room for environmental determinants in addition to genetic background. Several twin studies of tuberculosis have favored some genetic factors in clinical tuberculosis, but their evidence is mitigated by the many biases underlying such studies. Though very little work has been done on the genetics of leishmaniasis in man, experimental studies in mice have begun to unravel mechanisms controlling successive steps in the course of both L. donovani and L. torpica infections. It is suggested that future work should concentrate on moving from genetics to biochemical genetics in the mouse, should extend family studies in conjunction with markers in man, and should place high priority on confirmation of reported leprosy type discordance among monozygous twins.</p>
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