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Genetic variations in interleukin-12B in allergic rhinitis
Ping Wei1,2,3,4, Wei Kou5,6,7,8, Cheng Zhang9,10,11,12
1Department of Otolaryngology, The Children's Hospital of Chongqing Medical University, Chongqing, 136# Zhongshaner Road, Chongqing, 400014, China. entweiweidoctor@gmail.com.
Immunologic Research
|December 15, 2015
Summary
Single nucleotide polymorphisms in the Interleukin (IL)-12B gene are associated with allergic rhinitis (AR). Specific IL-12B gene variations influence immune responses, suggesting a role in AR susceptibility.
Area of Science:
- Immunogenetics
- Allergology
Background:
- Interleukin (IL)-12B plays a crucial role in immune responses against allergens.
- Allergic rhinitis (AR) is a common allergic condition affecting a significant portion of the population.
Purpose of the Study:
- To investigate the association between single nucleotide polymorphisms (SNPs) in the IL-12B gene and AR in a Chinese Han population.
- To explore the functional impact of identified IL-12B gene polymorphisms on immune mediator expression.
Main Methods:
- Genotyping of IL-12B SNPs (rs6887695, rs10045431, rs3212227, rs3212217, rs2082412) using PCR-based methods in 543 AR patients and 600 controls.
- Quantification of IL-12B mRNA expression in peripheral blood mononuclear cells (PBMCs) via quantitative real-time PCR.
- Measurement of interferon (IFN)-γ and IL-4 levels using enzyme-linked immunosorbent assay (ELISA).
Main Results:
- The rs3212227 genotype (CC) and C allele frequencies were significantly higher in AR patients compared to controls (p c = 8.55 × 10(-4) and p c = 4.20 × 10(-4), respectively).
- Healthy individuals with the CC genotype of rs3212227 showed reduced IL-12 mRNA expression after peptidoglycan stimulation.
- AR patients with the CC genotype exhibited decreased IFN-γ production and increased IL-4 expression compared to other genotypes.
Conclusions:
- The IL-12B gene is implicated in mediating susceptibility to allergic rhinitis.
- The rs3212227 polymorphism in IL-12B may influence AR risk by altering immune responses, specifically the balance between Th1 (IFN-γ) and Th2 (IL-4) cytokines.
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