02547nas a2200445   4500000000100000008004100001260003700042653001500079653001000094653000900104653002200113653001200135653001100147653002500158653001100183653001900194653003800213653001300251653004000264653001100304653001200315653000900327653001600336653001600352100001900368700001500387700001400402700001800416700001200434700001600446700001800462700001200480700002000492245007800512856009100590300001100681490000700692520138800699022001402087       2011                            d  c2011 OctbScieloaRio de Janeiro10aAdolescent10aAdult10aAged10aAged, 80 and over10aAlleles10aBrazil10aCase-Control Studies10aFemale10aGene Frequency10aGenetic Predisposition to Disease10agenotype10aHistocompatibility Antigens Class I10aHumans10aleprosy10aMale10aMiddle Aged10aYoung Adult1 aFranceschi DSA1 aTsuneto LT1 aMazini PS1 aSacramento WS1 aReis PG1 aRudnick CCC1 aClementino SL1 aSell AM1 aVisentainer JEL00aClass-I human leukocyte alleles in leprosy patients from Southern Brazil.  uhttp://www.scielo.br/scielo.php?script=sci_arttext&pid=S0037-86822011000500018&nrm=iso  a616-200 v443 a<p><b>INTRODUCTION: </b>The present study was designed to investigate a possible role of HLA (histocompatibility leucocyte antigen) class-I alleles (HLA-A, -B, and -C) in leprosy patients from Southern Brazil.</p><p><b>METHODS: </b>Two hundred and twenty-five patients with leprosy and 450 individuals for the control group were involved in this research. HLA genotyping was performed through PCR-SSO protocols (One Lambda, USA); the frequency of these alleles was calculated in each group by direct counting, and the frequencies were then compared.</p><p><b>RESULTS: </b>There was an association between HLA-A*11 (6.9% vs 4.1%, p=0.0345, OR=1.72, 95% CI=1.05-2.81), HLA-B*38 (2.7% vs. 1.1%, p=0.0402, OR=2.44, 95% CI=1.05-5.69), HLA-C*12 (9.4% vs. 5.4%, p=0.01, OR=1.82, 95% CI=1.17-2.82), and HLA-C*16 (3.1% vs. 6.5%, p=0.0124, OR=0.47, 95% CI=0.26-0.85) and leprosy per se. In addition, HLA-B*35, HLA-C*04, and HLA-C*07 frequencies were different between lepromatous (LL) and tuberculoid (TT) patients. However, after adjusting for the number of alleles compared, Pc values became nonsignificant.</p><p><b>CONCLUSIONS: </b>Although our results do not support the previous findings that HLA class-I alleles play a role in leprosy pathogenesis, we suggest new studies because of the importance of the association between the HLA and KIR in the innate immune response to leprosy.</p>  a1678-9849