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Scientific article
English

Danger signaling through the inflammasome acts as a master switch between tolerance and sensitization

Published inThe Journal of immunology, vol. 180, no. 9, p. 5826-5832
Publication date2008
Abstract

Efficient priming of adaptive immunity depends on danger signals provided by innate immune pathways. As an example, inflammasome-mediated activation of caspase-1 and IL-1beta is crucial for the development of reactive T cells targeting sensitizers like dinitrofluorobenzene (DNFB). Surprisingly, DNFB and dinitrothiocyanobenzene provide cross-reactive Ags yet drive opposing, sensitizing vs tolerizing, T cell responses. In this study, we show that, in mice, inflammasome-signaling levels can be modulated to turn dinitrothiocyanobenzene into a sensitizer and DNFB into a tolerizer, and that it correlates with the IL-6 and IL-12 secretion levels, affecting Th1, Th17, and regulatory T cell development. Hence, our data provide the first evidence that the inflammasome can define the type of adaptive immune response elicited by an Ag, and hint at new strategies to modulate T cell responses in vivo.

Keywords
  • Animals
  • Antigens/immunology
  • Caspase 1/immunology
  • Cross Reactions/drug effects/immunology
  • Dinitrobenzenes/pharmacology
  • Dinitrofluorobenzene/pharmacology
  • Humans
  • Immune Tolerance/drug effects/immunology
  • Immunity, Innate/drug effects/immunology
  • Inflammation/immunology
  • Interleukin-1beta/immunology
  • Interleukin-2/immunology
  • Interleukin-6/immunology
  • Mice
  • Signal Transduction/drug effects/immunology
  • T-Lymphocytes, Regulatory/immunology
  • Th1 Cells/immunology
Citation (ISO format)
WATANABE, Hideki et al. Danger signaling through the inflammasome acts as a master switch between tolerance and sensitization. In: The Journal of immunology, 2008, vol. 180, n° 9, p. 5826–5832. doi: 10.4049/jimmunol.180.9.5826
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Article (Accepted version)
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Identifiers
ISSN of the journal0022-1767
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