title: Study of killer immunoglobulin-like receptor genes and human leukocyte antigens class I ligands in a Caucasian Brazilian population with Crohn's disease and ulcerative colitis.
abstract: Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases of the bowel, of unknown origin. Exposure to specific environmental factors by genetically susceptible individuals, leading to an inadequate response of the immune system, is one of the potential explanations for the occurrence of these diseases. Natural killer cells are part of the innate immune system recognizing class I HLA (human leukocyte antigen) molecules on target cells through their membrane receptors. The main receptors of the natural killer cells are the killer immunoglobulinlike receptors (KIRs). Our study aimed to evaluate the association between the KIR genes in patients with inflammatory bowel diseases and healthy controls. We typed 15 KIR genes and HLA class I ligands in 248 unrelated Brazilian Caucasians, of which 111 had UC and 137 had CD, and 250 healthy controls by polymerase chain reaction using sequence-specific oligonucleotides and sequence-specific primers. We found an increase in KIR2DL2 in controls (inflammatory bowel disease [IBD]: p < 0.001; UC: p = 0.01; CD: p = not significant [NS]). The genotype 2DL2+/HLA-C lys(80)+ was also more common in controls (IBD: p = 0.005; UC: p = 0.01; CD: p = NS); as well as 2DL1+/HLA-C Asn(80)+ (IBD: p = 0.026; UC: p = NS;CD: p = NS). The imbalance between activating and inhibitory KIR and HLA ligands may explain, at least in part, the pathogenesis of these inflammatory bowel diseases.
authors.affiliation: Postgraduate Course in Medical Sciences, Faculty of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Wilson
authors.forename: Mariana
authors.initials: M
authors.lastname: Jobim
authors.forename: Luiz Fernando
authors.initials: LF
authors.lastname: Jobim
authors.forename: Pamela
authors.initials: P
authors.lastname: Portela
authors.forename: Patrícia H
authors.initials: PH
authors.lastname: Salim
authors.forename: Mário A
authors.initials: MA
authors.lastname: Rosito
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Damin
authors.forename: Cristina
authors.initials: C
authors.lastname: Flores
authors.forename: Alessandra
authors.initials: A
authors.lastname: Peres
authors.forename: Marta Brenner
authors.initials: MB
authors.lastname: Machado
authors.forename: José Artur Bogo
authors.initials: JA
authors.lastname: Chies
authors.forename: Gilberto
authors.initials: G
authors.lastname: Schwartsmann
authors.forename: Rafael
authors.initials: R
authors.lastname: Roesler
mesh_terms: D000328:Adult; D001938:Brazil; D003093:Colitis, Ulcerative / Q000453:epidemiology / Q000235:genetics*; D003424:Crohn Disease / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005805:Genes, MHC Class I / Q000235:genetics*; D006801:Humans; D008297:Male; D054340:Receptors, KIR / Q000235:genetics*; D044465:White People
chemical_list: D054340:Receptors, KIR