SynthesisZeitschrift fur Rheumatologie2014
Chemokine receptor 5 Δ32 polymorphism and systemic lupus erythematosus, vasculitis, and primary Sjogren's syndrome. Meta-analysis of possible associations.
Synthesis in Zeitschrift fur Rheumatologie, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis of SLC22A4 and RUNX1 polymorphisms : Associations with rheumatoid arthritis susceptibility.Zeitschrift fur Rheumatologie · 2015Pooled it
- CCR5Δ32 in Brazil: Impacts of a European Genetic Variant on a Highly Admixed Population.Frontiers in immunology · 2021Review
- Gq-Coupled Receptors in Autoimmunity.Journal of immunology research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study was to determine whether the functional chemokine receptor 5 delta32 (CCR5-Δ32) polymorphism is associated with susceptibility to systemic lupus erythematosus (SLE), vasculitis, and primary Sjogren's syndrome (pSS).
resultsA total of 12 studies were analyzed, including 5 on SLE, 5 on vasculitis, and 2 on pSS, encompassing 1881 patients and 2391 controls. Meta-analysis indicated no association between SLE and the CCR5-Δ32 allele (OR 0.842, 95 % CI 0.793-1.804, p = 0.657), and no association between the CCR5-Δ32 allele and SLE in Europeans (OR 0.647, 95 % CI 0.306-1.368, p = 0.255). Meta-analysis of the CCR5-Δ32 allele and the Δ32Δ32 + Δ32 W genotype showed no association with lupus nephritis (LN; OR 1.771, 95 % CI 0.475-6.595, p = 0.395; OR 2.192, 95 % CI 0.182-26.42, p = 0.537, respectively). In addition, meta-analysis revealed no association between the CCR5-Δ32 allele and vasculitis in all study subjects and in Europeans (OR 1.241, 95 % CI 0.951-1.620, p = 0.111; OR 1.359, 95 % CI 0.803-2.303, p = 0.254, respectively). However, the overall OR for the CCR5-Δ32 allele was significantly higher in Kawasaki disease (KD; OR 1.746, 95 % CI 1.003-2.955, p = 0.038) and the meta-analysis of the Δ32Δ32 + Δ32 W genotype showed a trend indicating an association with KD (OR 1.683, 95 % CI 0.921-3.077, p = 0.091). No association was found between the CCR5-Δ32 polymorphism and pSS.
conclusionThis meta-analysis demonstrates that the CCR5-Δ32 polymorphism is associated with KD, but does not facilitate susceptibility to SLE, LN, or pSS.
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Registered trials
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