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Related Experiment Video

Updated: Feb 24, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

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Effect of Interferon-γ Polymorphisms on Ankylosing Spondylitis: A Case-Control Study.

Haitao Xu¹, Bo Li²

¹Department of Orthopedics, The Yongchuan Hospital of Chongqing Medical University, Chongqing, China (mainland).

Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

|August 27, 2017

Summary

Interferon-gamma (IFN-γ) rs2430561 polymorphism increases ankylosing spondylitis (AS) risk in Chinese individuals. This genetic variation is linked to higher IFN-γ levels, suggesting a role in AS development.

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Published on: June 14, 2018

Area of Science:

Immunogenetics
Rheumatology
Molecular Biology

Background:

Ankylosing spondylitis (AS) is a chronic inflammatory disease.
The role of interferon-gamma (IFN-γ) in AS pathogenesis is not fully understood.
Genetic variations in IFN-γ may influence susceptibility to AS.

Purpose of the Study:

To investigate the association between IFN-γ gene polymorphisms and expression and AS susceptibility in a Chinese population.
To determine if specific IFN-γ genotypes are linked to altered IFN-γ serum levels in AS patients.

Main Methods:

Genotyping of IFN-γ polymorphisms (rs1861493, rs2430561) using PCR and sequencing.
Analysis of genotype distribution and Hardy-Weinberg equilibrium in 89 AS patients and 106 controls.
Quantification of serum IFN-γ levels via ELISA.
Statistical analysis using χ² test and odds ratios (OR) with 95% confidence intervals (95%CI).

Main Results:

The TT genotype and T allele of IFN-γ rs2430561 were significantly more frequent in AS patients than in controls (P=0.04 and P=0.03, respectively).
rs2430561 polymorphism was associated with an increased risk of AS (OR=2.54 for TT genotype, OR=1.60 for T allele).
Serum IFN-γ levels were elevated in AS patients, and expression correlated with rs2430561 genotypes.

Conclusions:

The IFN-γ rs2430561 polymorphism is a potential risk factor for AS in the Chinese population.
This genetic variation may contribute to AS susceptibility by modulating IFN-γ expression levels.
Further research is warranted to elucidate the precise mechanisms linking IFN-γ to AS pathogenesis.