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Updated: Sep 12, 2026
A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
Association of TLR-2 23 bp ins/del polymorphism (rs111200466) with susceptibility and clinical severity in ankylosing
Vinay Gopalaswamy1, Subrat Pradhan2, Saumya Ranjan Tripathy1
1Department of Clinical Immunology and Rheumatology, S.C.B. Medical College, Cuttack 753007, Odisha, India.
Background:
Ankylosing spondylitis (AS) is an inflammatory disorder exacerbated by the innate immune response. A 23-bp ins/del polymorphism at the 5'-untranslated region of the TLR-2 gene (rs111200466) is linked to varying expression levels of inflammatory cytokines, crucial in AS pathogenesis. This study examined the association between the TLR-2 (rs111200466) polymorphism and AS susceptibility and clinical severity.
Materials And Methods:
We enrolled 251 patients meeting the Modified New York Criteria for AS and 250 age- and sex-matched healthy controls from a similar region. Disease activity indices, including BASDAI, BASFI, ASDAS-CRP, and ASDAS-ESR, were measured, and haematological and biochemical parameters were quantified using standard methods. The TLR-2 (rs111200466) polymorphism was genotyped using PCR. Serum TNF-α and IL-17 levels were measured using ELISA.
Results:
Of 251 patients, 98% were men with a median age of 31 years. The ins/del and del/del genotypes were more common in AS patients than controls (ins/del: OR = 1.62, p = 0.03; del/del: OR = 4.24, p = 0.004). The minor allele 'del' was significantly more prevalent in AS patients (OR = 1.94, p = 0.0002). The del/del genotype was linked to higher ESR, CRP, TNF-α, IL-17, and disease severity indices like BASDAI, ASDAS-ESR, and ASDAS-CRP. Serum TNF-α positively correlated with ESR (r = 0.45, p < 0.0001), CRP (r = 0.33, p = 0.0002), BASDAI (r = 0.27, p = 0.002), ASDAS-CRP (r = 0.42, p < 0.0001), and ASDAS-ESR (r = 0.47, p < 0.0001).
Conclusions:
The TLR-2 (rs111200466) polymorphism exhibits a higher prevalence in AS patients and is associated with an inflammatory phenotype and high disease activity. This suggests a potential role in the severity of AS.
