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Crohn's disease associated CARD15 (NOD2) variants are not involved in the susceptibility to type 1 diabetes

Ghandil, P; Chelala, C; Dubois-Laforgue, D; Senee, V; Caillat-Zucman, S; Kockum, I; Luthman, Holger LU ; Nerup, J; Pociot, F and Timsit, J, et al. (2005) In Molecular Genetics and Metabolism 86(3). p.379-383
Abstract
Three variants in the caspase recruitment domain 15/nucleotide-binding oligomerization domain 2 (CARD15/NOD2) gene have been shown to be associated with Crohn's disease (CD). There is a strong support for shared genetic determinants between various autoimmune and inflammatory diseases. In particular, linkage of type 1 diabetes (T1D) and other autoimmune and inflammatory diseases has been reported on chromosome 16, encompassing the region containing the CARD15 gene. We therefore considered this gene as a good candidate for the T1D locus mapped to this region, and we tested the three CARD15 variants in the susceptibility to T I D in two independent settings: family based association analysis in Scandinavian multiplex families that we... (More)
Three variants in the caspase recruitment domain 15/nucleotide-binding oligomerization domain 2 (CARD15/NOD2) gene have been shown to be associated with Crohn's disease (CD). There is a strong support for shared genetic determinants between various autoimmune and inflammatory diseases. In particular, linkage of type 1 diabetes (T1D) and other autoimmune and inflammatory diseases has been reported on chromosome 16, encompassing the region containing the CARD15 gene. We therefore considered this gene as a good candidate for the T1D locus mapped to this region, and we tested the three CARD15 variants in the susceptibility to T I D in two independent settings: family based association analysis in Scandinavian multiplex families that we previously showed to be linked to this region, and case/control association study in a large cohort of French diabetic patients. We found no evidence for association of these variants with T1D overall, nor in subgroups of patients with or without the major risk genotypes at HLA-DRB1, at insulin (INS), or positive or negative for autoantibodies specific to other autoimmune diseases. Our results do not support a role for CD-associated CARD15 variants in the susceptibility to T1D, and suggest that another gene is responsible for the shared susceptibility between autoimmune and inflammatory diseases mapping to this region. (Less)
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Contribution to journal
publication status
published
subject
keywords
Crohn's disease, genetic variant, association, type 1 diabetes, genetics
in
Molecular Genetics and Metabolism
volume
86
issue
3
pages
379 - 383
publisher
Elsevier
external identifiers
  • pmid:16198136
  • wos:000233327600007
  • scopus:27644588763
ISSN
1096-7192
DOI
10.1016/j.ymgme.2005.07.029
language
English
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yes
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bdcc5b26-4bf2-403e-b2f5-751146d8e866 (old id 212918)
date added to LUP
2007-08-07 13:15:39
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2017-01-01 04:23:10
@article{bdcc5b26-4bf2-403e-b2f5-751146d8e866,
  abstract     = {Three variants in the caspase recruitment domain 15/nucleotide-binding oligomerization domain 2 (CARD15/NOD2) gene have been shown to be associated with Crohn's disease (CD). There is a strong support for shared genetic determinants between various autoimmune and inflammatory diseases. In particular, linkage of type 1 diabetes (T1D) and other autoimmune and inflammatory diseases has been reported on chromosome 16, encompassing the region containing the CARD15 gene. We therefore considered this gene as a good candidate for the T1D locus mapped to this region, and we tested the three CARD15 variants in the susceptibility to T I D in two independent settings: family based association analysis in Scandinavian multiplex families that we previously showed to be linked to this region, and case/control association study in a large cohort of French diabetic patients. We found no evidence for association of these variants with T1D overall, nor in subgroups of patients with or without the major risk genotypes at HLA-DRB1, at insulin (INS), or positive or negative for autoantibodies specific to other autoimmune diseases. Our results do not support a role for CD-associated CARD15 variants in the susceptibility to T1D, and suggest that another gene is responsible for the shared susceptibility between autoimmune and inflammatory diseases mapping to this region.},
  author       = {Ghandil, P and Chelala, C and Dubois-Laforgue, D and Senee, V and Caillat-Zucman, S and Kockum, I and Luthman, Holger and Nerup, J and Pociot, F and Timsit, J and Julier, C},
  issn         = {1096-7192},
  keyword      = {Crohn's disease,genetic variant,association,type 1 diabetes,genetics},
  language     = {eng},
  number       = {3},
  pages        = {379--383},
  publisher    = {Elsevier},
  series       = {Molecular Genetics and Metabolism},
  title        = {Crohn's disease associated CARD15 (NOD2) variants are not involved in the susceptibility to type 1 diabetes},
  url          = {http://dx.doi.org/10.1016/j.ymgme.2005.07.029},
  volume       = {86},
  year         = {2005},
}