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Aim <p>Systemic lupus erythematosus (SLE) is a complex autoimmune disease involving both genetic and environmental factors. A 32-bp deletion polymorphism (Δ32, rs333) in the C-C chemokine receptor type 5 (<i>CCR5</i>; MIM: 601373) results in a non-functional receptor and alters immune-related gene expression, suggesting its potential role in SLE pathogenesis. However, findings from previous studies have been inconsistent. This meta-analysis therefore aimed to clarify the association between the rs333 and susceptibility to SLE by synthesizing all available genetic data.</p> Methods <p>This study was conducted in accordance with the PRISMA guidelines. Eligible studies were identified by searching ten databases. Three genetic models (heterozygous, dominant, and allelic) were analysed using random- or fixed-effects models based on heterogeneity assessments. The wt/wt genotype and wt allele served as references.</p> Results <p>The initial search of the databases yielded 124 articles. Ultimately, eight case-control studies involving 1323 SLE patients and 1724 controls were included. No significant association was found between the <i>CCR5</i>-Δ32 variant and SLE risk in any genetic model (heterozygous: OR = 0.95, 95% CI: 0.58–1.54, <i>p</i> = 0.851; dominant: OR = 0.99, 95% CI: 0.60–1.65, <i>p</i> = 0.989; allelic: OR = 1.03, 95% CI: 0.62–1.70, <i>p</i> = 0.889), despite significant heterogeneity between studies (I²=68.8–74.4%). No evidence of publication bias was found.</p> Conclusion <p>Despite strong biological plausibility, this meta-analysis found no significant association between the rs333 and susceptibility to SLE, a finding consistent with null results reported in multiple sclerosis. Although limitations of the included studies preclude definitive conclusions, the cumulative evidence suggests that the rs333 is unlikely to be a primary genetic determinant of SLE risk.</p>

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A meta-analysis on association between chemokine receptor 5 delta32 polymorphism and risk of systemic lupus erythematosus

  • 期刊论文

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  • 发表日期：

    2025年11月18日

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  • Nazanin Akbari,
  • Mostafa Saadat

摘要

Aim

Systemic lupus erythematosus (SLE) is a complex autoimmune disease involving both genetic and environmental factors. A 32-bp deletion polymorphism (Δ32, rs333) in the C-C chemokine receptor type 5 (CCR5; MIM: 601373) results in a non-functional receptor and alters immune-related gene expression, suggesting its potential role in SLE pathogenesis. However, findings from previous studies have been inconsistent. This meta-analysis therefore aimed to clarify the association between the rs333 and susceptibility to SLE by synthesizing all available genetic data.

Methods

This study was conducted in accordance with the PRISMA guidelines. Eligible studies were identified by searching ten databases. Three genetic models (heterozygous, dominant, and allelic) were analysed using random- or fixed-effects models based on heterogeneity assessments. The wt/wt genotype and wt allele served as references.

Results

The initial search of the databases yielded 124 articles. Ultimately, eight case-control studies involving 1323 SLE patients and 1724 controls were included. No significant association was found between the CCR5-Δ32 variant and SLE risk in any genetic model (heterozygous: OR = 0.95, 95% CI: 0.58–1.54, p = 0.851; dominant: OR = 0.99, 95% CI: 0.60–1.65, p = 0.989; allelic: OR = 1.03, 95% CI: 0.62–1.70, p = 0.889), despite significant heterogeneity between studies (I²=68.8–74.4%). No evidence of publication bias was found.

Conclusion

Despite strong biological plausibility, this meta-analysis found no significant association between the rs333 and susceptibility to SLE, a finding consistent with null results reported in multiple sclerosis. Although limitations of the included studies preclude definitive conclusions, the cumulative evidence suggests that the rs333 is unlikely to be a primary genetic determinant of SLE risk.