File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The Bcl10-Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation

TitleThe Bcl10-Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation
Authors
Issue Date2006
Citation
Journal of Experimental Medicine, 2006, v. 203, n. 2, p. 337-347 How to Cite?
AbstractMast 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.
Persistent Identifierhttp://hdl.handle.net/10722/292570
ISSN
2023 Impact Factor: 12.6
2023 SCImago Journal Rankings: 6.838
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKlemm, Stefanie-
dc.contributor.authorGutermuth, Jan-
dc.contributor.authorHültner, Lothar-
dc.contributor.authorSparwasser, Tim-
dc.contributor.authorBehrendt, Heidrun-
dc.contributor.authorPeschel, Christian-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorJakob, Thilo-
dc.contributor.authorRuland, Jürgen-
dc.date.accessioned2020-11-17T14:56:45Z-
dc.date.available2020-11-17T14:56:45Z-
dc.date.issued2006-
dc.identifier.citationJournal of Experimental Medicine, 2006, v. 203, n. 2, p. 337-347-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/292570-
dc.description.abstractMast 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.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleThe Bcl10-Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1084/jem.20051982-
dc.identifier.pmid16432253-
dc.identifier.pmcidPMC2118204-
dc.identifier.scopuseid_2-s2.0-33344479146-
dc.identifier.volume203-
dc.identifier.issue2-
dc.identifier.spage337-
dc.identifier.epage347-
dc.identifier.isiWOS:000235707700013-
dc.identifier.f10001021643-
dc.identifier.issnl0022-1007-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats