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Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism

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Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism. / Mahnke, Justus ; Schumacher, Valéa; Ahrens, Stefanie; Käding, Nadja; Feldhoff, Lea Marie; Huber, Magdalena; Rupp, Jan; Raczkowski, Friederike; Mittrücker, Hans-Willi.

in: SCI REP-UK, Jahrgang 6, 20.10.2016, S. 35521.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Mahnke, J, Schumacher, V, Ahrens, S, Käding, N, Feldhoff, LM, Huber, M, Rupp, J, Raczkowski, F & Mittrücker, H-W 2016, 'Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism', SCI REP-UK, Jg. 6, S. 35521. https://doi.org/10.1038/srep35521

APA

Mahnke, J., Schumacher, V., Ahrens, S., Käding, N., Feldhoff, L. M., Huber, M., Rupp, J., Raczkowski, F., & Mittrücker, H-W. (2016). Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism. SCI REP-UK, 6, 35521. https://doi.org/10.1038/srep35521

Vancouver

Mahnke J, Schumacher V, Ahrens S, Käding N, Feldhoff LM, Huber M et al. Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism. SCI REP-UK. 2016 Okt 20;6:35521. https://doi.org/10.1038/srep35521

Bibtex

@article{f1c66e85c1094853afad3e3f0106cc18,
title = "Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism",
abstract = "The transcription factor Interferon Regulatory Factor 4 (IRF4) is essential for TH2 and TH17 cell formation and controls peripheral CD8(+) T cell differentiation. We used Listeria monocytogenes infection to characterize the function of IRF4 in TH1 responses. IRF4(-/-) mice generated only marginal numbers of listeria-specific TH1 cells. After transfer into infected mice, IRF4(-/-) CD4(+) T cells failed to differentiate into TH1 cells as indicated by reduced T-bet and IFN-γ expression, and showed limited proliferation. Activated IRF4(-/-) CD4(+) T cells exhibited diminished uptake of the glucose analog 2-NBDG, limited oxidative phosphorylation and strongly reduced aerobic glycolysis. Insufficient metabolic adaptation contributed to the limited proliferation and TH1 differentiation of IRF4(-/-) CD4(+) T cells. Our study identifies IRF4 as central regulator of TH1 responses and cellular metabolism. We propose that this function of IRF4 is fundamental for the initiation and maintenance of all TH cell responses.",
author = "Justus Mahnke and Val{\'e}a Schumacher and Stefanie Ahrens and Nadja K{\"a}ding and Feldhoff, {Lea Marie} and Magdalena Huber and Jan Rupp and Friederike Raczkowski and Hans-Willi Mittr{\"u}cker",
year = "2016",
month = oct,
day = "20",
doi = "10.1038/srep35521",
language = "English",
volume = "6",
pages = "35521",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Interferon Regulatory Factor 4 controls TH1 cell effector function and metabolism

AU - Mahnke, Justus

AU - Schumacher, Valéa

AU - Ahrens, Stefanie

AU - Käding, Nadja

AU - Feldhoff, Lea Marie

AU - Huber, Magdalena

AU - Rupp, Jan

AU - Raczkowski, Friederike

AU - Mittrücker, Hans-Willi

PY - 2016/10/20

Y1 - 2016/10/20

N2 - The transcription factor Interferon Regulatory Factor 4 (IRF4) is essential for TH2 and TH17 cell formation and controls peripheral CD8(+) T cell differentiation. We used Listeria monocytogenes infection to characterize the function of IRF4 in TH1 responses. IRF4(-/-) mice generated only marginal numbers of listeria-specific TH1 cells. After transfer into infected mice, IRF4(-/-) CD4(+) T cells failed to differentiate into TH1 cells as indicated by reduced T-bet and IFN-γ expression, and showed limited proliferation. Activated IRF4(-/-) CD4(+) T cells exhibited diminished uptake of the glucose analog 2-NBDG, limited oxidative phosphorylation and strongly reduced aerobic glycolysis. Insufficient metabolic adaptation contributed to the limited proliferation and TH1 differentiation of IRF4(-/-) CD4(+) T cells. Our study identifies IRF4 as central regulator of TH1 responses and cellular metabolism. We propose that this function of IRF4 is fundamental for the initiation and maintenance of all TH cell responses.

AB - The transcription factor Interferon Regulatory Factor 4 (IRF4) is essential for TH2 and TH17 cell formation and controls peripheral CD8(+) T cell differentiation. We used Listeria monocytogenes infection to characterize the function of IRF4 in TH1 responses. IRF4(-/-) mice generated only marginal numbers of listeria-specific TH1 cells. After transfer into infected mice, IRF4(-/-) CD4(+) T cells failed to differentiate into TH1 cells as indicated by reduced T-bet and IFN-γ expression, and showed limited proliferation. Activated IRF4(-/-) CD4(+) T cells exhibited diminished uptake of the glucose analog 2-NBDG, limited oxidative phosphorylation and strongly reduced aerobic glycolysis. Insufficient metabolic adaptation contributed to the limited proliferation and TH1 differentiation of IRF4(-/-) CD4(+) T cells. Our study identifies IRF4 as central regulator of TH1 responses and cellular metabolism. We propose that this function of IRF4 is fundamental for the initiation and maintenance of all TH cell responses.

U2 - 10.1038/srep35521

DO - 10.1038/srep35521

M3 - SCORING: Journal article

C2 - 27762344

VL - 6

SP - 35521

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

ER -