Genetics/Genomes/Proteomics/Metabolomics

Effect of the PTPN22 and INS Risk Genotypes on the Progression to Clinical Type 1 Diabetes After the Initiation of β-Cell Autoimmunity

  1. Johanna Lempainen1,2⇓,
  2. Robert Hermann1,
  3. Riitta Veijola3,
  4. Olli Simell2,
  5. Mikael Knip4,5,6 and
  6. Jorma Ilonen1,7
  1. 1Immunogenetics Laboratory, University of Turku, Turku, Finland
  2. 2Department of Pediatrics, University of Turku, Turku, Finland
  3. 3Department of Pediatrics, University of Oulu, Oulu, Finland
  4. 4Department of Pediatrics, Tampere University Hospital, Tampere, Finland
  5. 5Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland
  6. 6Folkhälsan Research Center, Helsinki, Finland
  7. 7Department of Clinical Microbiology, University of Eastern Finland, Kuopio, Finland
  1. Corresponding author: Johanna Lempainen, johanna.lempainen{at}utu.fi.
Diabetes 2012 Apr; 61(4): 963-966. https://doi.org/10.2337/db11-0386

Article Figures & Tables

Figures

  • FIG. 1.
    FIG. 1.

    Kaplan-Meier survival analysis shows the effects of the PTPN22 1858TT (solid line), 1858CT (dotted line), and 1858CC (dashed line) genotypes on the progression to clinical T1D after the appearance of the first biochemically defined autoantibody (AAB).

Tables

  • TABLE 1
  • TABLE 2
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Diabetes: 61 (4)

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April 2012, 61(4)
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Effect of the PTPN22 and INS Risk Genotypes on the Progression to Clinical Type 1 Diabetes After the Initiation of β-Cell Autoimmunity
Johanna Lempainen, Robert Hermann, Riitta Veijola, Olli Simell, Mikael Knip, Jorma Ilonen
Diabetes Apr 2012, 61 (4) 963-966; DOI: 10.2337/db11-0386
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