PuSH - Publikationsserver des Helmholtz Zentrums München: Kruppel-like factor KLF10 targets transforming growth factor-beta1 to regulate CD4<sup>+</sup> CD25<sup>-</sup> T cells and T regulatory cells.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Cao, Z.* ; Wara, A.K.* ; Icli, B.* ; Sun, X.* ; Packard, R.R.* ; Esen, F.* ; Stapleton, C.J.* ; Subramaniam, M.* ; Kretschmer, K.* ; Apostolou, I.* ; von Boehmer, H.* ; Hansson, G.K.* ; Spelsberg, T.C.* ; Libby, P.* ; Feinberg, M.W.*

Kruppel-like factor KLF10 targets transforming growth factor-beta1 to regulate CD4⁺ CD25^- T cells and T regulatory cells.

J. Biol. Chem. 284, 24914-24924 (2009)

DOI

PMC

Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.

Abstract
Metriken
Zusatzinfos

CD4(+)CD25(+) regulatory T cells (T regs) play a major role in the maintenance of self-tolerance and immune suppression, although the mechanisms controlling T reg development and suppressor function remain incompletely understood. Herein, we provide evidence that Kruppel-like factor 10 (KLF10/TIEG1) constitutes an important regulator of T regulatory cell suppressor function and CD4(+)CD25(-) T cell activation through distinct mechanisms involving transforming growth factor (TGF)-beta1 and Foxp3. KLF10 overexpressing CD4(+)CD25(-) T cells induced both TGF-beta1 and Foxp3 expression, an effect associated with reduced T-Bet (Th1 marker) and Gata3 (Th2 marker) mRNA expression. Consistently, KLF10(-/-) CD4(+)CD25(-) T cells have enhanced differentiation along both Th1 and Th2 pathways and elaborate higher levels of Th1 and Th2 cytokines. Furthermore, KLF10(-/-) CD4(+)CD25(-) T cell effectors cannot be appropriately suppressed by wild-type T regs. Surprisingly, KLF10(-/-) T reg cells have reduced suppressor function, independent of Foxp3 expression, with decreased expression and elaboration of TGF-beta1, an effect completely rescued by exogenous treatment with TGF-beta1. Mechanistic studies demonstrate that in response to TGF-beta1, KLF10 can transactivate both TGF-beta1 and Foxp3 promoters, implicating KLF10 in a positive feedback loop that may promote cell-intrinsic control of T cell activation. Finally, KLF10(-/-) CD4(+)CD25(-) T cells promoted atherosclerosis by approximately 2-fold in ApoE(-/-)/scid/scid mice with increased leukocyte accumulation and peripheral pro-inflammatory cytokines. Thus, KLF10 is a critical regulator in the transcriptional network controlling TGF-beta1 in both CD4(+)CD25(-) T cells and T regs and plays an important role in regulating atherosclerotic lesion formation in mice.

Impact Factor

Scopus SNIP

Altmetric

0.000

2.120

PuSH - Publikationsserver des Helmholtz Zentrums München

Kruppel-like factor KLF10 targets transforming growth factor-beta1 to regulate CD4+ CD25- T cells and T regulatory cells.

Kruppel-like factor KLF10 targets transforming growth factor-beta1 to regulate CD4⁺ CD25^- T cells and T regulatory cells.