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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

Z. Vrabelova, Z. Hrotekova, Z. Hladikova, K. Bohmova, K. Stechova, J. Michalek

. 2008 ; 67 (4) : 404-410.

Jazyk angličtina Země Velká Británie

Perzistentní odkaz   https://www.medvik.cz/link/bmc11003237

Grantová podpora
NR9355 MZ0 CEP - Centrální evidence projektů

Digitální knihovna NLK
Plný text - Článek
Zdroj

E-zdroje

NLK Free Medical Journals od 1997 do Před 1 rokem
Medline Complete (EBSCOhost) od 1972-01-01 do Před 1 rokem
Wiley Online Library (archiv) od 1997-01-01 do 2012-12-31
Wiley Free Content od 1997 do Před 1 rokem

Odkazy

Knihovny.cz E-zdroje

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.

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$a Libá, Zuzana. $7 xx0190588 $u Department of Pediatrics; Children's Neurology Department, University Hopital Motol, Prague; Cell Immunotherapy Center, Masaryk University, Brno, Czech Republic
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$a 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.
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