Cited by 17Diabetes and associated disordersT-cell and B-cell ImmunologyImmunotherapy and Immune Responses

Functional evaluation of the role of C-type lectin domain family 16A at the chromosome 16p13 locus

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Zouk, H, D'Hennezel, E, Du, X, Ounissi-Benkalha, H, Piccirillo, C A, Polychronakos, C·2014·Clinical and Experimental Immunology

Abstract

The type 1 diabetes-associated 16p13 locus contains the CLEC16A gene. Its preferential immune cell expression suggests involvement in autoimmunity. Given its elevated expression in dendritic and B cells - known professional antigen-presenting cells (APCs) - we hypothesize that C-type lectin domain family 16 member A (CLEC16A) may be involved in T cell co-stimulation and consequent activation and proliferation. We also sought to identify CLEC16A's subcellular localization. The effect of the CLEC16A knock-down (KD) on B cell co-stimulation and activation of T cells was tested in human lymphoblastoid cell lines (LCLs) by co-culture with CD4(+) T cells. T cell activation and proliferation were determined by flow-cytometric analysis of CD69 and CD25 expression and carboxyfluorescein succinimidyl ester (CFSE) dilution, respectively. CLEC16A subcellular localization in K562 cells was examined by immunofluorescence. We show that the CLEC16A KD did not affect the tested indices of lymphoblastoid cell line (LCL) APC capacity. Additionally, the percentage of activated T cells following LCL co-culture was not affected significantly by the CLEC16A KD. T cells co-cultured with KD or control LCLs also exhibited similar cell division profiles. CLEC16A co-localized with an endoplasmic reticulum (ER) marker, suggesting that it may be an ER protein. In conclusion, CLEC16A may not be involved in T cell co-stimulation. Additional studies on CLEC16A, accounting for its ER localization, are needed…

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Crossref · 10.1111/cei.12240

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  • These data are similar to those obtained upon CLEC16A siRNA knockdown in human B cells serving as antigen presenting cells.

    “These data are similar to those obtained upon CLEC16A siRNA knockdown in human B cells serving as antigen presenting cells34.”

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  1. Ormerod, 2008, Cell proliferation, 80

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Authors
Zouk, H., D'Hennezel, E., Du, X., Ounissi-Benkalha, H., Piccirillo, C. A., & Polychronakos, C.
Affiliations
  • Montreal Children's Hospital (CA)
  • McGill University Health Centre (CA)
  • Endocrine Genetics Laboratory, McGill University Health Center, Montreal Children's Hospital Research Institute, Montreal, QC, Canada
Corresponding author
Polychronakos, C
Venue
Clinical and Experimental Immunology
Published
2014-02-04
Volume
175
Issue
3
Pages
485-497
ISSN
  • 0009-9104 (ISSN-L)
  • 1365-2249
OpenAlex
W1930060214
Cited by
17
References
45
Citations by year
2025: 1 · 2023: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 1 · 2016: 2 · 2015: 5 · 2014: 1
FWCI
1.76
Type
journal article
Language
en
Open access
Locations
  • Clinical & Experimental Immunology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Juvenile Diabetes Research Foundation
  • Fonds de Recherche en Santé du Québec
  • Montreal Children's Hospital Research Institute
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords
CLEC16A, type 1 diabetes, T cell costimulation, antigen-presenting cells, B cells, dendritic cells, T cell activation, T cell proliferation, endoplasmic reticulum localization, subcellular localization, gene knockdown, lymphoblastoid cell lines, autoimmunity
MeSH terms
Antigen-Presenting Cells, B-Lymphocytes, Chromosomes, Human, Pair 16, Endoplasmic Reticulum, Humans, Leukocytes, Mononuclear, Lymphocyte Activation, Monosaccharide Transport Proteins, T-Lymphocytes, Coculture Techniques, K562 Cells, Protein Transport, Lectins, C-Type, Gene Knockdown Techniques, Genetic Loci

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