A20-Deficient Mast Cells Exacerbate Inflammatory Responses In Vivo

Klaus Heger, Kaat Fierens, J. Christoph Vahl, Attila Aszodi, Katrin Peschke, Dominik Schenten, Hamida Hammad, Rudi Beyaert, Dieter Saur, Geert van Loo, Axel Roers, Bart N. Lambrecht, Mirjam Kool, Marc Schmidt-Supprian

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


Mast cells are implicated in the pathogenesis of inflammatory and autoimmune diseases. However, this notion based on studies in mast cell-deficient mice is controversial. We therefore established an in vivo model for hyperactive mast cells by specifically ablating the NF-κB negative feedback regulator A20. While A20 deficiency did not affect mast cell degranulation, it resulted in amplified pro-inflammatory responses downstream of IgE/FcεRI, TLRs, IL-1R, and IL-33R. As a consequence house dust mite- and IL-33-driven lung inflammation, late phase cutaneous anaphylaxis, and collagen-induced arthritis were aggravated, in contrast to experimental autoimmune encephalomyelitis and immediate anaphylaxis. Our results provide in vivo evidence that hyperactive mast cells can exacerbate inflammatory disorders and define diseases that might benefit from therapeutic intervention with mast cell function.

Original languageEnglish (US)
Article numbere1001762
JournalPLoS biology
Issue number1
StatePublished - Jan 2014

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Agricultural and Biological Sciences(all)


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