IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cellsCitation formats

  • External authors:
  • Ilgiz A Mufazalov
  • Carsten Schelmbauer
  • Tommy Regen
  • Janina Kuschmann
  • Florian Wanke
  • Laureen A Gabriel
  • Judith Hauptmann
  • Florian C Kurschus
  • Ari Waisman

Standard

IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells. / Mufazalov, Ilgiz A; Schelmbauer, Carsten; Regen, Tommy; Kuschmann, Janina; Wanke, Florian; Gabriel, Laureen A; Hauptmann, Judith; Müller, Werner; Pinteaux, Emmanuel; Kurschus, Florian C; Waisman, Ari.

In: The EMBO Journal, 2016.

Research output: Contribution to journalArticle

Harvard

Mufazalov, IA, Schelmbauer, C, Regen, T, Kuschmann, J, Wanke, F, Gabriel, LA, Hauptmann, J, Müller, W, Pinteaux, E, Kurschus, FC & Waisman, A 2016, 'IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells' The EMBO Journal. https://doi.org/10.15252/embj.201694615

APA

Mufazalov, I. A., Schelmbauer, C., Regen, T., Kuschmann, J., Wanke, F., Gabriel, L. A., ... Waisman, A. (2016). IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells. The EMBO Journal. https://doi.org/10.15252/embj.201694615

Vancouver

Mufazalov IA, Schelmbauer C, Regen T, Kuschmann J, Wanke F, Gabriel LA et al. IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells. The EMBO Journal. 2016. https://doi.org/10.15252/embj.201694615

Author

Mufazalov, Ilgiz A ; Schelmbauer, Carsten ; Regen, Tommy ; Kuschmann, Janina ; Wanke, Florian ; Gabriel, Laureen A ; Hauptmann, Judith ; Müller, Werner ; Pinteaux, Emmanuel ; Kurschus, Florian C ; Waisman, Ari. / IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells. In: The EMBO Journal. 2016.

Bibtex

@article{78ec50a3a2384cd3a5fee47cd2648bf3,
title = "IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells",
abstract = "Interleukin-1 (IL-1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL-1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1β expression by myeloid cells in the draining lymph nodes. This myeloid-derived IL-1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM-CSF(+) Th17 cell subset, thereby enhancing its encephalitogenic potential. Lack of expansion of GM-CSF-producing Th17 cells led to ameliorated disease in mice deficient for IL-1R1 specifically in T cells. Importantly, pathogenicity of IL-1R1-deficient T cells was fully restored by IL-23 polarization and expansion in vitro Therefore, our data demonstrate that IL-1 functions as a mitogenic mediator of encephalitogenic Th17 cells rather than qualitative inducer of their generation.",
author = "Mufazalov, {Ilgiz A} and Carsten Schelmbauer and Tommy Regen and Janina Kuschmann and Florian Wanke and Gabriel, {Laureen A} and Judith Hauptmann and Werner M{\"u}ller and Emmanuel Pinteaux and Kurschus, {Florian C} and Ari Waisman",
note = "{\circledC} 2016 The Authors.",
year = "2016",
doi = "10.15252/embj.201694615",
language = "English",
journal = "EMBO Journal",
issn = "0261-4189",
publisher = "Springer Nature",

}

RIS

TY - JOUR

T1 - IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells

AU - Mufazalov, Ilgiz A

AU - Schelmbauer, Carsten

AU - Regen, Tommy

AU - Kuschmann, Janina

AU - Wanke, Florian

AU - Gabriel, Laureen A

AU - Hauptmann, Judith

AU - Müller, Werner

AU - Pinteaux, Emmanuel

AU - Kurschus, Florian C

AU - Waisman, Ari

N1 - © 2016 The Authors.

PY - 2016

Y1 - 2016

N2 - Interleukin-1 (IL-1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL-1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1β expression by myeloid cells in the draining lymph nodes. This myeloid-derived IL-1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM-CSF(+) Th17 cell subset, thereby enhancing its encephalitogenic potential. Lack of expansion of GM-CSF-producing Th17 cells led to ameliorated disease in mice deficient for IL-1R1 specifically in T cells. Importantly, pathogenicity of IL-1R1-deficient T cells was fully restored by IL-23 polarization and expansion in vitro Therefore, our data demonstrate that IL-1 functions as a mitogenic mediator of encephalitogenic Th17 cells rather than qualitative inducer of their generation.

AB - Interleukin-1 (IL-1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL-1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1β expression by myeloid cells in the draining lymph nodes. This myeloid-derived IL-1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM-CSF(+) Th17 cell subset, thereby enhancing its encephalitogenic potential. Lack of expansion of GM-CSF-producing Th17 cells led to ameliorated disease in mice deficient for IL-1R1 specifically in T cells. Importantly, pathogenicity of IL-1R1-deficient T cells was fully restored by IL-23 polarization and expansion in vitro Therefore, our data demonstrate that IL-1 functions as a mitogenic mediator of encephalitogenic Th17 cells rather than qualitative inducer of their generation.

U2 - 10.15252/embj.201694615

DO - 10.15252/embj.201694615

M3 - Article

JO - EMBO Journal

JF - EMBO Journal

SN - 0261-4189

ER -