02330nas a2200325 4500000000100000008004100001260001300042653001200055653002700067653001900094653002400113653003800137653001900175653001100194653001000205653002400215653002500239653002500264653003000289100001100319700002400330700001500354700001400369700001400383245009100397300001000488490000700498520148500505022001401990 1993 d c1993 Sep10aAlleles10aDisease Susceptibility10aGene Frequency10aGenes, MHC Class II10aGenetic Predisposition to Disease10aHLA-D Antigens10aHumans10aIndia10aLeprosy, Borderline10aLeprosy, lepromatous10aLeprosy, Tuberculoid10apolymerase chain reaction1 aRani R1 aFernandez-ViƱa M A1 aZaheer S A1 aBeena K R1 aStastny P00aStudy of HLA class II alleles by PCR oligotyping in leprosy patients from north India. a133-70 v423 a

Host factors seem to play an important role in determining the immune response and the differential manifestations of lepromatous (LL) and tuberculoid (TT) leprosy. In order to investigate the role of immunogenetic factors in determining the form of leprosy, the HLA class II alleles of DRB1, DRB3, DRB5, DQA1, DQB1 and DPB1 were studied by a PCR oligotyping technique in 93 patients and 47 healthy controls. DRB1*1501 and DRB1*1502 (two of five tested subsets of the serologically defined DR2) accounted for 81.5% of the multibacillary patients (relative risk 16.3) and 60.7% of the TT patients (relative risk 5.7) compared to 21.3% in normal, ethnically- and geographically-matched controls. The much stronger association of DRB1*1501 with the multibacillary form than with the TT type of leprosy suggests a possible role in the differential immune response to M. leprae antigens. DQB1*0601 was found significantly more often than in controls throughout the leprosy spectrum, while DQA1*0103 was most frequent in the LL group and DQA1*0102 was selectively increased in the borderline lepromatous (BL) patients. On the other hand, DRB1*0701, DQB1*0201 and DQA1*0201 were decreased in the multibacillary leprosy patients (MLP) compared to TT patients and controls, and DQB1*0503 was selectively decreased in TT patients, suggesting that these HLA alleles might play a role in modulating the immune response that determines the form of leprosy that develops in each patient.

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