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Polymorphisms of B-lymphocyte-associated genes CD20 and FCRL5 are associated with susceptibility to autoimmune thyroid diseases.

Authors :
Wu Y
Cai T
Xu W
Yang X
Gu P
Zhang J
Source :
Human immunology [Hum Immunol] 2024 Oct 25; Vol. 85 (6), pp. 111165. Date of Electronic Publication: 2024 Oct 25.
Publication Year :
2024
Publisher :
Ahead of Print

Abstract

Background: Recent studies have confirmed that B cell-related genes CD20 and FCRL5 may be involved in the pathogenesis of autoimmune thyroid diseases (AITDs). However, there is a lack of comprehensive genetic susceptibility studies on this subject.<br />Objective: The purpose of this study was to investigate the relationship of CD20 and FCRL5 gene polymorphisms with AITD susceptibility.<br />Methods: A total of 1740 subjects were recruited from the Chinese Han population. They consisted of 1007 patients with AITD and 633 healthy controls. Multiplex polymerase chain reaction (PCR) combined with high-throughput sequencing was used to genotype four screened single nucleotide polymorphisms (SNPs). The four SNPs were rs7126354 of CD20 and rs6667109, rs6692977 and rs3811035 of FCRL5.<br />Results: The minor allele frequency of rs7126354 was significantly lower in patients with AITD and Hashimoto's thyroiditis (HT) than in healthy controls (P = 0.031; P = 0.017). The minor allele frequency of rs6667109 was significantly higher in the Graves' disease (GD) subgroup than in the healthy control group (P = 0.029). In the Log-additive model, rs6667109 in the GD group also showed an increased risk of onset disease.<br />Conclusions: This study presents robust evidence of a genetic association of CD20 and FCRL5 with AITDs. The C allele of CD20 rs7126354 is a protective factor for HT susceptibility. The A allele of FCRL5 rs6667109 is a risk factor for the susceptibility to GD.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024. Published by Elsevier Inc.)

Details

Language :
English
ISSN :
1879-1166
Volume :
85
Issue :
6
Database :
MEDLINE
Journal :
Human immunology
Publication Type :
Academic Journal
Accession number :
39461276
Full Text :
https://doi.org/10.1016/j.humimm.2024.111165