Class II allele and haplotype frequencies in Mexican systemic lupus erythematosus patients: The relevance of considering homologous chromosomes in determining susceptibility

The aim of the present study was to deter,mine the relevant major histocomp atibility complex (MHC) class II alleles in the generic susceptibility to s ystemic lupus erythematosus (SLE) in Mexican Mestizo patients. We examined the gene and haplotype frequencies of the HLA-DRB1, DQA1 and DQB1 alleles b y polymerase chain reaction-sequence-specific oligonucleotide probes in 81 Mexican SLE Mestizo patients and 99 ethnically matched controls. We found a significantly increased frequency of the HLA-DRB1*0301 (p(c) = 0.031, odds ratio = 2.63) allele and significantly decreased frequencies of the DRB1*0 802 (p(c) = 0.035) and DRB1*1101 (p(c) = 0.037) alleles in the SLE group. H aplotype analysis showed increased frequencies of DRB1*0301-DQA1*0501-DQB1* 0201 (p(c) = 0.017, odds ratio = 2.97), and decreased frequency of DRB1-080 2-DQA1*0401-DQB1*0402 (p(c) = 0.034) in SLE patients. The most frequently d etected haplotypes in SLE patients showed different haplotypic combinations in the homologous chromosome from those found in controls. Thus, the combi nations detected in SLE patients were either not detected in the control gr oup or infrequently found. The results suggest that the DRB1*0301 is the pr incipal class II allele associated with the genetic susceptibility to SLE i n Mexican patients and that the presence of a specific haplotype of the hom ologous chromosome in patients with DRB1*0407-DQA1*03-DQB1*0302 and DRB1*15 01-DQA1*0102-DQB1*0602 haplotypes could have an additive effect on the susc eptibility to the disease. Finally, the low frequency of the DRB1*0301 and DRB1*1501 alleles in the control population suggests that the genetic admix ture between Mexican Indians and Caucasian populations was an event that co uld have increased the risk of Mexicans to develop SLE. Human Immunology 62 , 814-820 (2001). (C) American Society for Histocompatibility and Immunogen etics, 2001. Published by Elsevier Science Inc.