Association of alleles at polymorphic sites in the Osteopontin encoding gene in young type 1 diabetic patients
The Osteopontin (OPN) encoding gene, SPP1, can be considered as a candidate for genetic susceptibility to type 1 diabetes (T1D) because of its known function in immune response and inflammation. This work aimed to evaluate the role of SPP1 gene in susceptibility to T1D. Patients (238: 130 male, 108...
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 131(2009), 1 vom: 15. Apr., Seite 84-91 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2009
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Autoantibodies HLA-DQ Antigens HLA-DQ alpha-Chains HLA-DQ beta-Chains HLA-DQA1 antigen HLA-DQB1 antigen Membrane Glycoproteins SPP1 protein, human Osteopontin mehr... |
| Zusammenfassung: | The Osteopontin (OPN) encoding gene, SPP1, can be considered as a candidate for genetic susceptibility to type 1 diabetes (T1D) because of its known function in immune response and inflammation. This work aimed to evaluate the role of SPP1 gene in susceptibility to T1D. Patients (238: 130 male, 108 female) and unaffected adult control individuals (137: 68 males and 69 females) have been genotyped for three variants in the SPP1 gene: -156 (G/GG) and -66 (T/G) in the promoter and a biallelic ins/del variant (TG/TGTG) at +245 in the first intron. The G allele at the -66 SNP had significantly higher frequency in controls than T1D patients. Interestingly, case-control comparison in males showed no significant association, whereas the association was confirmed in females. These results suggest that SPP1 can play a role as susceptibility gene, possibly by a sex-specific mechanism acting in the autoimmune process |
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| Beschreibung: | Date Completed 01.05.2009 Date Revised 17.11.2011 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2008.11.004 |