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Updated: Nov 19, 2025

qKAT: Quantitative Semi-automated Typing of Killer-cell Immunoglobulin-like Receptor Genes
Published on: March 6, 2019
Association of KIR gene polymorphisms with Type 1 Diabetes: a meta-analysis
Samaneh Soltani1, Shayan Mostafaei2, Saeed Aslani3
1Rheumatology Research Center, Shariati Hospital, Tehran University of Medical Sciences, PO-BOX: 1411713137, Kargar Ave., Tehran, Iran.
Purpose:
Type 1 Diabetes (T1D) is a T cell-mediated disease, in which autoimmune destruction of insulin-producing β-cells in pancreatic islets occurs. In recent decades, the role of Killer cell immunoglobulin-like receptor (KIR) gene polymorphisms in susceptibility to T1D has been demonstrated in an increased number of studies. Nonetheless, inconsistency has been observed in the results of performed association studies. To comprehensively clarify the association among KIR gene polymorphisms and the risk of T1D, this meta-analysis on the previously published association studies was carried out via incorporating multiple research.
Methods:
No publication has been recorded from Nov 2017 until July 2020 about the KIR genes and T1D. The PubMed/MEDLINE and Scopus databases were systematically searched up to November 2017 to identify investigations on the impact of the polymorphisms of KIR genes on susceptibility to T1D. The odds ratio (OR) with a 95% confidence interval (95% CI) was calculated. Funnel plot and Egger test were used to assess the publication bias. Thirteen qualified published case-control articles were found for evaluation in this meta-analysis.
Results:
Our results show statistical significance between the genetic variations in the KIR2DL1 (OR = 0.42, 95% CI = 0.23-0.77; P = 0.005), KIR2DL2 (OR = 1.15, 95% CI = 1.00-1.32; P = 0.048), and KIR2DL5 (OR = 0.86, 95% CI = 0.75-0.98; P = 0.03) with susceptibility to T1D.
Conclusions:
This meta-analysis study provides reliable evidence that KIR gene polymorphisms may contribute to T1D risk. KIR 2DL1 and 2DL5 genes might be considered as a protective factor for T1D, while 2DL2 seemed to be a susceptibility factor.
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