ArticleJournal of translational autoimmunity2021
The 3p21.31 genetic locus promotes progression to type 1 diabetes through the CCR2/CCL2 pathway.
Article in Journal of translational autoimmunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Role of the Neanderthal Genome in Genetic Susceptibility to COVID-19: 3p21.31 Locus in the Spotlight.Biochemical genetics · 2024Review
- The association of rs17713054 with Neanderthal origin at 3p21.31 locus with the severity of COVID-19 in Iranian patients.Scientific reports · 2024Article
- Integrating Multimorbidity into a Whole-Body Understanding of Disease Using Spatial Genomics.Results and problems in cell differentiation · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
Multiple cross-sectional and longitudinal studies have shown that serum levels of the chemokine ligand 2 (CCL-2) are associated with type 1 diabetes (T1D), although the direction of effect differs. We assessed CCL-2 serum levels in a longitudinal cohort to clarify this association, combined with genetic data to elucidate the regulatory role of CCL-2 in T1D pathogenesis. The Diabetes Autoimmunity Study in the Young (DAISY) followed 310 subjects with high risk of developing T1D. Of these, 42 became persistently seropositive for islet autoantibodies but did not develop T1D (non-progressors); 48 did develop T1D (progressors). CCL-2 serum levels among the three study groups were compared using linear mixed models adjusting for age, sex, HLA genotype, and family history of T1D. Summary statistics were obtained from the CCL-2 protein quantitative trait loci (pQTL) and
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