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Killer immunoglobulin-like receptor repertoire analysis in a Caucasian Spanish cohort with inflammatory bowel disease.

Authors :
López‐Hernández, Ruth
Campillo, Jose A.
Legaz, Isabel
Valdés, Mariano
Salama, Hortensia
Boix, Francisco
Hernández‐Martínez, AM
Eguia, Jorge
González‐Martínez, G
Moya‐Quiles, Maria R.
Minguela, Alfredo
García‐Alonso, Ana
Carballo, Fernando
Muro, Manuel
Source :
Microbiology & Immunology; Nov2016, Vol. 60 Issue 11, p787-792, 6p
Publication Year :
2016

Abstract

ABSTRACT Immunological molecules are implicated in inflammatory disorders, including inflammatory bowel disease (IBD; Crohn disease [CD] and ulcerative colitis [UC]). Killer cell immunoglobulin-like receptors (KIRs) are also genetically variable proteins involved in immune function. They are expressed by NK cells and certain T lymphocytes, regulate specificity and function by interaction with HLA Class I molecules, may be either inhibitory or activating and are polymorphic both in terms of alleles and haplotype gene content. Genetic associations between activating KIRs and certain autoimmune and inflammatory diseases have been reported; however, a possible association between KIR and IBD remains unclear. The aim of this study was to determine the relationship between KIR repertoire and IBD pathologies in a Spanish cohort. KIR variability was analyzed using PCR-sequence specific oligonucleotide probes (SSOP). Inhibitory KIR2DL5 was found more frequently in UC and IBD patient groups than in healthy controls ( P = 0.028 and P = 0.01, respectively), as was activating KIR2DS1 ( P = 0.02, Pc > 0.05, UC vs. Controls; P = 0.001, Pc = 0.01, IBD vs Controls; P = 0.01, Pc > 0.05, Controls vs CR), KIR2DS5 ( P = 0.0028, Pc = 0.04, Controls vs UC; P = 0.0001, Pc = 0.0017, Controls vs IBD; P = 0.01, Pc > 0.05, Controls vs CD) and KIR3DS1 ( P = 0.012, Pc > 0.05, Controls vs IBD). Our data suggest that imbalance between activating and inhibitory KIR may partially explain the different pathogeneses of these IBDs and that there is a hypothetical role for the telomeric B region (which contains both KIR2DS5 and KIR2DS1) in these diseases. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03855600
Volume :
60
Issue :
11
Database :
Complementary Index
Journal :
Microbiology & Immunology
Publication Type :
Academic Journal
Accession number :
119974343
Full Text :
https://doi.org/10.1111/1348-0421.12447