InflammasomeIL-1Th17 response in allergic lung inflammation

Anne Gaelle Besnard, Dieudonnée Togbe, Isabelle Couillin, Zoming Tan, Song Guo Zheng, François Erard, Marc Le Bert, Valérie Quesniaux, Bernhard Ryffel

Research output: Contribution to journalReview article

98 Scopus citations

Abstract

Allergic asthma has increased dramatically in prevalence and severity over the last three decades. Both clinical and experimental data support an important role of Th2 cell response in the allergic response. Recent investigations revealed that airway exposure to allergen in sensitized individuals causes the release of ATP and uric acid, activating the NLRP3 inflammasome complex and cleaving pro-IL-1β to mature IL-1β through caspase-1. The production of pro-IL-1β requires a toll-like receptor (TLR) 4 signal which is provided by the allergen. IL-1β creates a pro-inflammatory milieu with the production of IL-6 and chemokines which mobilize neutrophils and enhance Th17 cell differentiation in the lung. Here, we review our results showing that NLRP3 inflammasome activation is required to develop allergic airway inflammation in mice and that IL-17 and IL-22 production by Th17 cells plays a critical role in established asthma. Therefore, inflammasome activation leading to IL-1β production contributes to the control of allergic asthma by enhancing Th17 cell differentiation.

Original languageEnglish (US)
Pages (from-to)3-10
Number of pages8
JournalJournal of Molecular Cell Biology
Volume4
Issue number1
DOIs
StatePublished - Feb 1 2012

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cell Biology

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    Besnard, A. G., Togbe, D., Couillin, I., Tan, Z., Zheng, S. G., Erard, F., Le Bert, M., Quesniaux, V., & Ryffel, B. (2012). InflammasomeIL-1Th17 response in allergic lung inflammation. Journal of Molecular Cell Biology, 4(1), 3-10. https://doi.org/10.1093/jmcb/mjr042