GM-CSF producing autoreactive CD4+ T cells in type 1 diabetes

Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 188(2018) vom: 10. März, Seite 23-30
1. Verfasser: Knoop, Jan (VerfasserIn)
Weitere Verfasser: Gavrisan, Anita, Kuehn, Denise, Reinhardt, Julia, Heinrich, Melanie, Hippich, Markus, Eugster, Anne, Ockert, Christian, Ziegler, Anette-Gabriele, Bonifacio, Ezio
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2018
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Autoreactive T cells Cytokines GM-CSF Memory CD4(+) T cell TH1 immunity Type 1 diabetes Autoantigens Granulocyte-Macrophage Colony-Stimulating Factor mehr... 83869-56-1 Proinsulin 9035-68-1 Glutamate Decarboxylase EC 4.1.1.15 glutamate decarboxylase 2
Beschreibung
Zusammenfassung:Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
The phenotype of autoreactive T cells in type 1 diabetes is described as Th1, Th17 and/or Th21, but is largely uncharacterized. We combined multi-parameter cytokine profiling and proliferation, and identified GM-CSF producing cells as a component of the response to beta cell autoantigens proinsulin and GAD65. Overall cytokine profiles of CD4+ T cell were not altered in type 1 diabetes. In contrast, patients with recent onset type 1 diabetes had increased frequencies of proinsulin-responsive CD4+CD45RA- T cells producing GM-CSF (p=0.002), IFNγ (p=0.004), IL-17A (p=0.008), IL-21 (p=0.011), and IL-22 (p=0.007), and GAD65-responsive CD4+CD45RA- T cells producing IL-21 (p=0.039). CD4+ T cells with a GM-CSF+IFNγ-IL-17A-IL-21-IL-22- phenotype were increased in patients for responses to both proinsulin (p=0.006) and GAD65 (p=0.037). GM-CSF producing T cells are a novel phenotype in the repertoire of T helper cells in type 1 diabetes and consolidate a Th1/Th17 pro-inflammatory pathogenesis in the disease
Beschreibung:Date Completed 22.04.2019
Date Revised 22.04.2019
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2017.12.002