Scientific article

IL-36R ligands are potent regulators of dendritic and T cells

Published inBlood, vol. 118, no. 22, p. 5813-5823
Publication date2011

IL-36α (IL-1F6), IL-36β (IL-1F8), and IL-36γ (IL-1F9) are members of the IL-1 family of cytokines. These cytokines bind to IL-36R (IL-1Rrp2) and IL-1RAcP, activating similar intracellular signals as IL-1, whereas IL-36Ra (IL-1F5) acts as an IL-36R antagonist (IL-36Ra). In this study, we show that both murine bone marrow-derived dendritic cells (BMDCs) and CD4(+) T lymphocytes constitutively express IL-36R and respond to IL-36α, IL-36β, and IL-36γ. IL-36 induced the production of proinflammatory cytokines, including IL-12, IL-1β, IL-6, TNF-α, and IL-23 by BMDCs with a more potent stimulatory effect than that of other IL-1 cytokines. In addition, IL-36β enhanced the expression of CD80, CD86, and MHC class II by BMDCs. IL-36 also induced the production of IFN-γ, IL-4, and IL-17 by CD4(+) T cells and cultured splenocytes. These stimulatory effects were antagonized by IL-36Ra when used in 100- to 1000-fold molar excess. The immunization of mice with IL-36β significantly and specifically promoted Th1 responses. Our data thus indicate a critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.

  • Animals
  • Bone Marrow Cells/drug effects/metabolism/physiology
  • Cells, Cultured
  • Dendritic Cells/drug effects/metabolism/physiology
  • Dose-Response Relationship, Drug
  • Drug Evaluation, Preclinical
  • Interleukin-1/pharmacology/physiology
  • Interleukins/pharmacology/physiology
  • Ligands
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Interleukin/agonists/antagonists & inhibitors/genetics/metabolism
  • Receptors, Interleukin-1/agonists/genetics/metabolism
  • T-Lymphocytes/drug effects/metabolism/physiology
Citation (ISO format)
VIGNE, Solenne et al. IL-36R ligands are potent regulators of dendritic and T cells. In: Blood, 2011, vol. 118, n° 22, p. 5813–5823. doi: 10.1182/blood-2011-05-356873
Main files (1)
Article (Published version)
ISSN of the journal0006-4971

Technical informations

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