A case-control study on correlation between the single nucleotide polymorphism of CLEC4E and the susceptibility to tuberculosis among Han people in Western China.
CLEC4E
Disease susceptibility
Single nucleotide polymorphisms
Tuberculosis
Journal
BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551
Informations de publication
Date de publication:
10 Aug 2021
10 Aug 2021
Historique:
received:
29
09
2020
accepted:
20
07
2021
entrez:
11
8
2021
pubmed:
12
8
2021
medline:
25
9
2021
Statut:
epublish
Résumé
Tuberculosis (TB) is one of the leading causes of morbidity and mortality in Western China. Preclinical studies have suggested the protective effect of the C-type lectin receptor of family 4 member E (CLEC4E) from TB. Herein, we investigated the association between CLEC4E gene variants and TB susceptibility in a western Chinese Han population. We genotyped four single nucleotide polymorphisms (SNPs) rs10841856, rs10770847, rs10770855 and rs4480590 in the CLEC4E gene using the improved multiplex ligation detection reaction (iMLDR) assay in 900 TB cases and 1534 healthy controls. After stratifying the whole data by sex, it was found that males exhibited mutant allele G of rs10841856 was more strongly associated with increased TB risk after Bonferroni correction (OR = 1.334, 95% CI: 1.142-1.560; P < 0.001 after adjusting for age; p = 0.001 after Bonferroni correction). The genetic model analysis found that rs10841856 was associated with the increased risk of TB among males under the dominant model (OR = 1.557, 95% CI = 1.228-1.984, P < 0.001 after adjusting for age, P < 0.001 after Bonferroni correction). Bioinformatics analysis suggested that rs10841856 might fall in putative functional regions and might be the expression quantitative trait loci (eQTL) for CLEC4E and long noncoding RNA RP11-561P12.5. Our study revealed that rs10841856 in the CLEC4E gene might be related to increased TB risk, especially the dominant genetic model among male Han individuals from Western China.
Sections du résumé
BACKGROUND
BACKGROUND
Tuberculosis (TB) is one of the leading causes of morbidity and mortality in Western China. Preclinical studies have suggested the protective effect of the C-type lectin receptor of family 4 member E (CLEC4E) from TB. Herein, we investigated the association between CLEC4E gene variants and TB susceptibility in a western Chinese Han population.
METHODS
METHODS
We genotyped four single nucleotide polymorphisms (SNPs) rs10841856, rs10770847, rs10770855 and rs4480590 in the CLEC4E gene using the improved multiplex ligation detection reaction (iMLDR) assay in 900 TB cases and 1534 healthy controls.
RESULTS
RESULTS
After stratifying the whole data by sex, it was found that males exhibited mutant allele G of rs10841856 was more strongly associated with increased TB risk after Bonferroni correction (OR = 1.334, 95% CI: 1.142-1.560; P < 0.001 after adjusting for age; p = 0.001 after Bonferroni correction). The genetic model analysis found that rs10841856 was associated with the increased risk of TB among males under the dominant model (OR = 1.557, 95% CI = 1.228-1.984, P < 0.001 after adjusting for age, P < 0.001 after Bonferroni correction). Bioinformatics analysis suggested that rs10841856 might fall in putative functional regions and might be the expression quantitative trait loci (eQTL) for CLEC4E and long noncoding RNA RP11-561P12.5.
CONCLUSIONS
CONCLUSIONS
Our study revealed that rs10841856 in the CLEC4E gene might be related to increased TB risk, especially the dominant genetic model among male Han individuals from Western China.
Identifiants
pubmed: 34376176
doi: 10.1186/s12879-021-06448-2
pii: 10.1186/s12879-021-06448-2
pmc: PMC8353747
doi:
Substances chimiques
CLEC4D protein, human
0
Lectins, C-Type
0
Receptors, Immunologic
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
788Subventions
Organisme : national natural science foundation of china
ID : 81472026
Organisme : science and technology project of tibet autonomous region
ID : XZ201901-GB-08
Informations de copyright
© 2021. The Author(s).
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