PMID- 20036705
OWN - NLM
STAT- MEDLINE
DCOM- 20100907
LR  - 20221207
IS  - 1879-1166 (Electronic)
IS  - 0198-8859 (Linking)
VI  - 71
IP  - 3
DP  - 2010 Mar
TI  - 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.
PG  - 293-7
LID - 10.1016/j.humimm.2009.12.006 [doi]
AB  - 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.
CI  - (c) 2010 American Society for Histocompatibility and Immunogenetics. Published by 
      Elsevier Inc. All rights reserved.
FAU - Wilson, Timothy J
AU  - Wilson TJ
AD  - Postgraduate Course in Medical Sciences, Faculty of Medicine, Federal University 
      of Rio Grande do Sul, Porto Alegre, Brazil.
FAU - Jobim, Mariana
AU  - Jobim M
FAU - Jobim, Luiz Fernando
AU  - Jobim LF
FAU - Portela, Pamela
AU  - Portela P
FAU - Salim, Patricia H
AU  - Salim PH
FAU - Rosito, Mario A
AU  - Rosito MA
FAU - Damin, Daniel C
AU  - Damin DC
FAU - Flores, Cristina
AU  - Flores C
FAU - Peres, Alessandra
AU  - Peres A
FAU - Machado, Marta Brenner
AU  - Machado MB
FAU - Chies, Jose Artur Bogo
AU  - Chies JA
FAU - Schwartsmann, Gilberto
AU  - Schwartsmann G
FAU - Roesler, Rafael
AU  - Roesler R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100108
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Receptors, KIR)
SB  - IM
MH  - Adult
MH  - Brazil
MH  - Colitis, Ulcerative/epidemiology/*genetics
MH  - Crohn Disease/epidemiology/*genetics
MH  - Female
MH  - Genes, MHC Class I/*genetics
MH  - Humans
MH  - Male
MH  - Receptors, KIR/*genetics
MH  - White People
EDAT- 2009/12/29 06:00
MHDA- 2010/09/08 06:00
CRDT- 2009/12/29 06:00
PHST- 2009/05/18 00:00 [received]
PHST- 2009/12/02 00:00 [revised]
PHST- 2009/12/17 00:00 [accepted]
PHST- 2009/12/29 06:00 [entrez]
PHST- 2009/12/29 06:00 [pubmed]
PHST- 2010/09/08 06:00 [medline]
AID - S0198-8859(09)00660-0 [pii]
AID - 10.1016/j.humimm.2009.12.006 [doi]
PST - ppublish
SO  - Hum Immunol. 2010 Mar;71(3):293-7. doi: 10.1016/j.humimm.2009.12.006. Epub 2010 
      Jan 8.