PMID- 20580654 OWN - NLM STAT- MEDLINE DCOM- 20101115 LR - 20100719 IS - 1879-1166 (Electronic) IS - 0198-8859 (Linking) VI - 71 IP - 8 DP - 2010 Aug TI - Association of killer cell immunoglobulin-like receptors and human leukocyte antigen-C genotypes in South Brazilian with type 1 diabetes. PG - 799-803 LID - 10.1016/j.humimm.2010.05.014 [doi] AB - Type 1 diabetes mellitus (T1D) is a multifactorial and chronic autoimmune disease caused by the deficiency of insulin synthesis and or by its secretion or action defects. Genetic and environmental factors are known to be involved in its pathogenesis. The human leukocyte antigen complex (human leukocyte antigen (HLA)) constitutes the most relevant region contributing with 50% of the inherited risk for T1D. Natural killer cells (NK) are part of the innate immune system recognizing class I HLA molecules on target cells through their membrane receptors, called killer immunoglobulin-like receptors (KIR). The aim of our study is to evaluate the association between the KIR genes and HLA alleles in patients with T1D and healthy controls. Two hundred forty-eight T1D patients and 250 healthy controls were typed for HLA and KIR genes by PCR-SSP. Our results showed an increase of C2 in controls (p = 0.002). The genotype 2DL1/C2+ was also more common in controls (p = 0.001), as well as haplotype association KIR2DL2/DR3/DR4+ and the combination with only DR3+ (p < 0.001; p < 0.001). The maximum protection was seen when KIR2DL2/DR3-were absent when the combination of KIR2DL1/C2+ were present (p < 0.001) and the maximum risk was observed when KIR2DL2/DR3/DR4+ were present in the absence of KIR2DL1/C2- (p = 0.005). Our results confirmed the association of the KIR2DL2/DR3 increasing risk for T1D and suggest a protective role of KIR2DL1/C2. CI - Copyright 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved. FAU - Jobim, Mariana AU - Jobim M AD - Department of Immunology, Hospital de Clinicas, Porto Alegre, Brazil; Postgraduate Course in Medical Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil. mjobim@hcpa.ufrgs.br FAU - Chagastelles, Pedro AU - Chagastelles P FAU - Salim, Patricia H AU - Salim PH FAU - Portela, Pamela AU - Portela P FAU - Wilson, Timothy J AU - Wilson TJ FAU - Curti, Alessandra G AU - Curti AG FAU - Jobim, Maria Regina AU - Jobim MR FAU - Joao, Daniele A AU - Joao DA FAU - Nardi, Nance Beyer AU - Nardi NB FAU - Tschiedel, Balduino AU - Tschiedel B FAU - Jobim, Luiz Fernando AU - Jobim LF FAU - Roesler, Rafael AU - Roesler R FAU - Schwartsmann, Gilberto AU - Schwartsmann G LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100516 PL - United States TA - Hum Immunol JT - Human immunology JID - 8010936 RN - 0 (HLA-C Antigens) RN - 0 (KIR2DL1 protein, human) RN - 0 (KIR2DL4 protein, human) RN - 0 (KIR3DL2 protein, human) RN - 0 (KIR3DL3 protein, human) RN - 0 (Receptors, KIR) RN - 0 (Receptors, KIR2DL1) RN - 0 (Receptors, KIR2DL4) RN - 0 (Receptors, KIR3DL2) SB - IM MH - Adolescent MH - Brazil MH - Chi-Square Distribution MH - Child MH - Child, Preschool MH - Diabetes Mellitus, Type 1/*genetics MH - Gene Frequency MH - Genetic Predisposition to Disease/*genetics MH - Genotype MH - HLA-C Antigens/*genetics MH - Haplotypes MH - Humans MH - Infant MH - Infant, Newborn MH - Polymerase Chain Reaction MH - Receptors, KIR/genetics MH - Receptors, KIR2DL1/*genetics MH - Receptors, KIR2DL4/genetics MH - Receptors, KIR3DL2/genetics EDAT- 2010/06/29 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/29 06:00 PHST- 2010/02/19 00:00 [received] PHST- 2010/02/19 00:00 [revised] PHST- 2010/05/12 00:00 [accepted] PHST- 2010/06/29 06:00 [entrez] PHST- 2010/06/29 06:00 [pubmed] PHST- 2010/11/16 06:00 [medline] AID - S0198-8859(10)00125-4 [pii] AID - 10.1016/j.humimm.2010.05.014 [doi] PST - ppublish SO - Hum Immunol. 2010 Aug;71(8):799-803. doi: 10.1016/j.humimm.2010.05.014. Epub 2010 May 16.