Abstract:
: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.
journal_name
PLoS Bioljournal_title
PLoS biologyauthors
Heger K,Fierens K,Vahl JC,Aszodi A,Peschke K,Schenten D,Hammad H,Beyaert R,Saur D,van Loo G,Roers A,Lambrecht BN,Kool M,Schmidt-Supprian Mdoi
10.1371/journal.pbio.1001762subject
Has Abstractpub_date
2014-01-01 00:00:00pages
e1001762issue
1eissn
1544-9173issn
1545-7885pii
PBIOLOGY-D-13-02581journal_volume
12pub_type
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