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
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18248531
DOI
10.1111/j.1365-3083.2008.02074.x
PII: SJI2074
Knihovny.cz E-resources
- MeSH
- CD4 Antigens analysis MeSH
- Diabetes Mellitus, Type 1 immunology MeSH
- Adult MeSH
- Forkhead Transcription Factors analysis MeSH
- Cells, Cultured MeSH
- Humans MeSH
- Adolescent MeSH
- Lymphocyte Count MeSH
- Flow Cytometry MeSH
- Interleukin-2 Receptor alpha Subunit analysis MeSH
- Interleukin-7 Receptor alpha Subunit analysis MeSH
- T-Lymphocytes, Regulatory immunology MeSH
- Risk Factors MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- CD4 Antigens MeSH
- Forkhead Transcription Factors MeSH
- FOXP3 protein, human MeSH Browser
- Interleukin-2 Receptor alpha Subunit MeSH
- Interleukin-7 Receptor alpha Subunit MeSH
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-gamma (IFN-gamma) 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 < or = 0.02). Individuals at increased HLA-associated genetic risk for T1D showed defects in Treg.
References provided by Crossref.org
Case report: type 1 diabetes in monozygotic quadruplets
