Scientific article
Open access

IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells

Published inBlood, vol. 120, no. 17, p. 3478-3487
Publication date2012

The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36β acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo.

  • Adaptive Immunity
  • Animals
  • Cell Differentiation
  • Cell Proliferation
  • Interleukin-1/immunology/pharmacology
  • Interleukin-12/immunology/pharmacology
  • Interleukin-2/biosynthesis/immunology
  • Lymphocyte Activation
  • Mice
  • Mice, Knockout
  • Mycobacterium bovis/immunology
  • Primary Cell Culture
  • Receptors, Interleukin-1/deficiency/genetics/immunology
  • Signal Transduction/genetics/immunology
  • Th1 Cells/cytology/immunology/microbiology
  • Tuberculosis/genetics/immunology/metabolism/veterinary
  • Swiss National Science Foundation - 3200A0-118196
Citation (ISO format)
VIGNE, Solenne et al. IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells. In: Blood, 2012, vol. 120, n° 17, p. 3478–3487. doi: 10.1182/blood-2012-06-439026
Main files (1)
Article (Published version)
ISSN of the journal0006-4971

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