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ITAM receptor signaling and the NLRP3 inflammasome in antifungal immunity.
J. Clin. Immunol. 30, 496-501 (2010)
Publ. Version/Full Text
DOI
PMC
Infections with fungi can cause systemic life-threatening diseases in immunocompromised individuals like cancer or AIDS patients. Recent work has uncovered essential roles for C-type lectin pattern recognition receptors, spleen tyrosine kinase (SYK) and the cytosolic NLRP3 inflammasome in innate antifungal immunity. Upon fungal infection, SYK is activated by several ITAM-containing or ITAM-coupled C-type lectin receptors on myeloid cells leading to the production of pro-inflammatory cytokines including IL-1beta to initiate antifungal responses. Mature IL-1beta production requires in addition to the synthesis of pro-IL-1beta a cleavage of the precursor protein by the inflammatory Caspase-1 which is controlled within the NLRP3 inflammasome. SCOPE: Here, we discuss how ITAM receptor signaling and NLRP3 cooperate for the induction of antifungal immunity.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
ITAM receptors; SYK; CARD9; inflammasome; NLRP3; IL-1 beta
ISSN (print) / ISBN
0271-9142
e-ISSN
1573-2592
Journal
Journal of Clinical Immunology
Quellenangaben
Volume: 30,
Issue: 4,
Pages: 496-501
Publisher
Springer
Publishing Place
New York, NY
Non-patent literature
Publications
Reviewing status
Peer reviewed