Adult-onset type 1 diabetes patients display decreased IGRP-specific Tr1 cells in blood

Copyright © 2015 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 161(2015), 2 vom: 14. Dez., Seite 270-7
Auteur principal: Chujo, Daisuke (Auteur)
Autres auteurs: Nguyen, Thien-Son, Foucat, Emile, Blankenship, Derek, Banchereau, Jacques, Nepom, Gerald T, Chaussabel, Damien, Ueno, Hideki
Format: Article en ligne
Langue:English
Publié: 2015
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't CD4 T cells Islet antigens Islet-specific glucose 6 phosphatase catalytic subunit-related protein T regulatory type 1 (Tr1) cells Type 1 diabetes Cytokines Insulin Protein Precursors plus... preproinsulin 61116-24-3 Glucose-6-Phosphatase EC 3.1.3.9 G6PC2 protein, human EC 3.1.3.9. GAD55, human EC 4.1.1.15 Glutamate Decarboxylase
Description
Résumé:Copyright © 2015 Elsevier Inc. All rights reserved.
The breakdown of immune tolerance against islet antigens causes type 1 diabetes (T1D). The antigens associated with adult-onset T1D (AT1D) remain largely undefined. It is possible that AT1D patients display a unique type of CD4(+) T cells specific for a certain islet antigen. Here we analyzed the cytokine production profiles of CD4(+) helper T (Th) cells that are specific for three islet antigens; GAD65, preproinsulin, and IGRP in patients with AT1D, juvenile-onset T1D (JT1D), and age-, gender- and human leukocyte antigen (HLA)-matched control adults. While IGRP-specific Th cells in AT1D patients were dominantly Th1 cells, IGRP-specific Th cells in control adults and JT1D patients were dominantly Th2 and T regulatory type 1 (Tr1) cells. Notably, the frequency of IGRP-specific Tr1 cells was significantly lower in AT1D patients than in control adults and JT1D patients. In conclusion, our study suggests that IGRP-specific Th cells play a unique pathogenic role in AT1D
Description:Date Completed 14.03.2016
Date Revised 23.11.2015
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2015.08.014