ArticlePloS one2015
Multiple Sclerosis Risk Allele in CLEC16A Acts as an Expression Quantitative Trait Locus for CLEC16A and SOCS1 in CD4+ T Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Polygenic risk scores and HLA class II variants are biomarkers of corticosteroid response in childhood nephrotic syndrome.Kidney international · 2026Article
- Endosome traffic in rheumatic diseases: mechanistic insights and therapeutic opportunities.Nature reviews. Rheumatology · 2026Review
- Polygenic Risk Scores and HLA Class II Variants are Biomarkers of Corticosteroid Response in Childhood Nephrotic Syndrome.medRxiv : the preprint server for health sciences · 2025Article
- Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025Review
- Review
- 3D genome organization and epigenetic regulation in autoimmune diseases.Frontiers in immunology · 2023Review
- Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences.Biomedicines · 2020Review
- Clarifying the function of genes at the chromosome 16p13 locus in type 1 diabetes: CLEC16A and DEXI.Genes and immunity · 2020Article
- 9q34 & 16p13 chromosome duplications in autism.AME case reports · 2020Article
- The type 1 diabetes candidate gene Dexi does not affect disease risk in the nonobese diabetic mouse model.Genes and immunity · 2020Article
- The Genetic Contribution to Type 1 Diabetes.Current diabetes reports · 2019Review
- The genetic architecture of helminth-specific immune responses in a wild population of Soay sheep (Ovis aries).PLoS genetics · 2019Article
- Negative Regulation of Cytokine Signaling in Immunity.Cold Spring Harbor perspectives in biology · 2018Review
- Genome-Wide Analysis in Brazilians Reveals Highly Differentiated Native American Genome Regions.Molecular biology and evolution · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For multiple sclerosis, genome wide association studies and follow up studies have identified susceptibility single nucleotide polymorphisms located in or near CLEC16A at chromosome 16p13.13, encompassing among others CIITA, DEXI and SOCS1 in addition to CLEC16A. These genetic variants are located in intronic or intergenic regions and display strong linkage disequilibrium with each other, complicating the understanding of their functional contribution and the identification of the direct causal variant(s). Previous studies have shown that multiple sclerosis-associated risk variants in CLEC16A act as expression quantitative trait loci for CLEC16A itself in human pancreatic β-cells, for DEXI and SOCS1 in thymic tissue samples, and for DEXI in monocytes and lymphoblastoid cell lines. Since T cells are major players in multiple sclerosis pathogenesis, we have performed expression analyses of the CIITA-DEXI-CLEC16A-SOCS1 gene cluster in CD4+ and CD8+ T cells isolated from multiple sclerosis patients and healthy controls. We observed a higher expression of SOCS1 and CLEC16A in CD4+ T cells in samples homozygous for the risk allele of CLEC16A rs12927355. Pair-wise linear regression analysis revealed high correlation in gene expression in peripheral T cells of CIITA, DEXI, CLEC16A and SOCS1. Our data imply a possible regulatory role for the multiple sclerosis-associated rs12927355 in CLEC16A.
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