Association of TLR-2 23 bp ins/del polymorphism (rs111200466) with susceptibility and clinical severity in ankylosing spondylitis: A hospital-based case-control study.
Sep 2026· Human Immunology· Vol 87 11, pp.
112069
· 0 citations· 34 references
Medicine
TL;DR
The TLR-2 (rs111200466) polymorphism exhibits a higher prevalence in AS patients and is associated with an inflammatory phenotype and high disease activity, which suggests a potential role in the severity of AS.
Abstract
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.
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