Volume 15, Issue 4 (1-2014)                   yafte 2014, 15(4): 5-13 | Back to browse issues page

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Shahsavar F, Azargoon A, Sabooteh T. Association of activating KIRs with susceptibility to tuberculosis in Lur population. yafte 2014; 15 (4) :5-13
URL: http://yafte.lums.ac.ir/article-1-1439-en.html
Abstract:   (8241 Views)
Background: Natural Killer (NK) cells, through mechanisms such as cytotoxicity and cytokine production, are among the first line of defence against infections. The ability of NK cytotoxicity is related to Killer cell immunoglobulin-like receptors (KIR) found on the cell surface. Interaction between KIRs and human leukocyte antigen (HLA) class I molecules regulate NK cells responses to eliminate infected cells. Therefore, in continuation of a preliminary study, the aim of this supplementary study was to investigate the impact of KIR genes, HLA ligand genes, and KIR-HLA combinations on susceptibility to tuberculosis (TB) in Lur population. Materials and Methods: The genomic DNA of 50 patients with TB from Lorestan province was genotyped for sixteen KIR genes and their five major HLA class I ligands by a polymerase chain reaction-sequence specific primers (PCR-SSP) assay. Finally, these results were compared with those of 100 healthy Lur individuals. Results: In this study, the frequency of KIR3DS1 was significantly higher in the control group than the patient group (45% vs. 24%, Pc=0.0204). Also, KIR3DS1+HLA-B Bw4Ile80 combination was more frequent in control individuals compared to TB patients (25% vs. 4%, Pc=0.0034). Conclusion: These findings imply a genetic imbalance between activating and inhibitory KIR genes and KIR-HLA combinations in TB patients of Lur population. Low level of activating KIRs and particularly KIR3DS1 and its combination with HLA-B Bw4Ile80 ligand might have an influence on the susceptibility to TB in Lur population. Indeed, these findings confirmed the results of our preliminary study.
Keywords: Tuberculosis, NK Cells, KIR, HLA.
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Type of Study: Research |
Received: 2014/01/18 | Accepted: 2014/01/18 | Published: 2014/01/18

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