01946nas a2200313 4500000000100000008004100001260001300042653001300055653001100068653002000079653003200099653001100131653001200142653003700154653000900191653001300200653002800213100001100241700001400252700001400266700001500280700001400295700001300309245007600322300001200398490000800410520120000418022001401618 1980 d c1980 Jun10aEpitopes10aFemale10aGenetic Markers10aHistocompatibility Antigens10aHumans10aleprosy10aMajor Histocompatibility Complex10aMale10aPedigree10aTuberculosis, Cutaneous1 aEden W1 aVries R R1 aMehra N K1 aVaidya M C1 aD'Amaro J1 aRood J J00aHLA segregation of tuberculoid leprosy: confirmation of the DR2 marker. a693-7010 v1413 a

Families with multiple cases of leprosy were tested for HLA (histocompatibility leukocyte antigen)-linked control of susceptibility to tuberculoid leprosy and association with HLA-DR2. Thirty-one non-HLA genetic markers were also examined for indications of non-HLA-linked genetic factors that might control susceptibility to tuberculoid leprosy. A significant (P = 0.002) preferential inheritance of HLA-DR2 by siblings affected with tuberculoid leprosy, but not by healthy siblings nor by siblings affected with lepromatous leprosy, was observed. In addition, combined family data showed a significant (P less than 0.0025) excess of identical HLA haplotypes inherited from healthy parents by siblings affected with tuberculoid leprosy. Segregation on non-HLA polymorphisms did not deviate significantly from what would have occured randomly. These data are compatible with a recessive inheritance of HLA-linked susceptibility to tuberculoid leprosy. The preferential segregation of DR2 observed in children with tuberculoid leprosy (P less than 0.001 for the combined data from India) indicates that the HLA-linked susceptibility gene is either DR2 or in linkage disequilibrium with it.

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