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CD 127− and FoxP3+ Expression on CD25+CD4+ T Regulatory Cells upon Specific Diabetogeneic Stimulation in High-risk Relatives of Type 1 Diabetes Mellitus Patients

  1. Z. Vrabelova1,2,3,
  2. Z. Hrotekova2,
  3. Z. Hladikova1,
  4. K. Bohmova1,
  5. K. Stechova1,
  6. J. Michalek3,4

Article first published online: 1 FEB 2008

DOI: 10.1111/j.1365-3083.2008.02074.x

Issue

Scandinavian Journal of Immunology

Scandinavian Journal of Immunology

Volume 67, Issue 4, pages 404–410, April 2008

Additional Information

How to Cite

Vrabelova, Z., Hrotekova, Z., Hladikova, Z., Bohmova, K., Stechova, K. and Michalek, J. (2008), CD 127− and FoxP3+ Expression on CD25+CD4+ T Regulatory Cells upon Specific Diabetogeneic Stimulation in High-risk Relatives of Type 1 Diabetes Mellitus Patients. Scandinavian Journal of Immunology, 67: 404–410. doi: 10.1111/j.1365-3083.2008.02074.x

Author Information

  1. 1

    Department of Pediatrics

  2. 2

    Children’s Neurology Department, University Hospital Motol, Prague

  3. 3

    Cell Immunotherapy Center, Masaryk University

  4. 4

    First Department of Pediatrics, University Hospital Brno, Brno, Czech Republic

*Z. Vrabelova, MD, Children’s Neurology Department, University Hospital Motol, V uvalu 84, Prague 150 06, Czech Republic. E-mail: zuzanavr@email.cz

Publication History

  1. Issue published online: 1 FEB 2008
  2. Article first published online: 1 FEB 2008
  3. Received 31 August 2007; Accepted in revised form 12 December 2007

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Abstract

Abnormalities in CD4+CD25+ regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. First-degree relatives of T1D patients are at increased risk especially when they carry certain HLA II haplotypes. Using two novel markers of CD4+CD25+ Treg (CD127− and FoxP3+ respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high-risk (according to HLA-linked risk) relatives of T1D patients and 14 age-matched healthy controls using a cytokine secretion assay based on interferon-γ (IFN-γ) production. High-risk relatives of T1D patients had significantly lower pre- and post-stimulatory number of CD127− Treg than that of healthy controls (P < 0.05). Labelling Treg with FoxP3+ demonstrated similar trend but did not reach statistical significance. Although the stimulation with diabetogenic autoantigens did not lead to a significant change in number of Treg in both groups, the defective function of Treg was performed by significantly higher activation of diabetogeneic T cells in high-risk relatives of T1D patients compared to healthy controls (P ≤ 0.02). Individuals at increased HLA-associated genetic risk for T1D showed defects in Treg.

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