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Klemm, S.* ; Gutermuth, J. ; Hültner, L. ; Sparwasser, T.* ; Behrendt, H. ; Peschel, C.* ; Mak, T.W.* ; Jakob, T. ; Ruland, J.*

The Bcl10-Malt1 complex segregates FcRI-mediated nuclear factor kB activation and cytokine production from mast cell degranulation.

J. Exp. Med. 203, 337-347 (2006)
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Mast cells are pivotal effector cells in IgE-mediated allergic inflammatory diseases. Central for mast cell activation are signals from the IgE receptor FcεRI, which induce cell degranulation with the release of preformed mediators and de novo synthesis of proinflammatory leukotrienes and cytokines. How these individual mast cell responses are differentially controlled is still unresolved. We identify B cell lymphoma 10 (Bcl10) and mucosa-associated lymphoid tissue 1 (Malt1) as novel key regulators of mast cell signaling. Mice deficient for either protein display severely impaired IgE-dependent late phase anaphylactic reactions. Mast cells from these animals neither activate nuclear factor κB (NF-κB) nor produce tumor necrosis factor α or interleukin 6 upon FcεRI ligation even though proximal signaling, degranulation, and leukotriene secretion are normal. Thus, Bcl10 and Malt1 are essential positive mediators of FcεRI-dependent mast cell activation that selectively uncouple NF-κB-induced proinflammatory cytokine production from degranulation and leukotriene synthesis. JEM © The Rockefeller University Press.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Journal Journal of Experimental Medicine
Quellenangaben Volume: 203, Issue: 2, Pages: 337-347 Article Number: , Supplement: ,
Publisher Rockefeller University Press
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Lung Health and Immunity (LHI)
Institute of Epidemiology (EPI)
Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)