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Open Access Green as soon as Postprint is submitted to ZB.
SYK kinase signaling and the NLRP3 inflammasome in antifungal immunity.
J. Mol. Med. 88, 745-752 (2010)
Host protection against fungi depends on intact innate and adaptive immune responses. Consistently, fungal infections can cause systemic life-threatening diseases in immunocomprimised individuals, suffering e.g. from cancer or AIDS. Recent work has uncovered essential roles for the spleen tyrosine kinase (SYK) and the cytosolic NLRP3 inflammasome for Interleukin-1beta (IL-1beta) production in innate antifungal immunity. Upon fungal infection, SYK is activated by several C-type lectin pattern recognition receptors on myeloid cells. Subsequently, SYK signals for the production of reactive oxygen species and for gene transcription to induce pro-inflammatory factors, including pro-IL-1beta to initiate antifungal responses. Mature IL-1beta production additionally requires cleavage of the pro-IL-1beta precursor protein by the inflammatory caspase-1 which is controlled within the NLRP3 inflammasome. Here, we discuss how SYK signaling cooperates with the NLRP3 inflammasome for IL-1beta production in antifungal immunity.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
ITAM receptors; SYK; CARD9; Inflammasome; NLRP3; IL-1β
ISSN (print) / ISBN
0946-2716
e-ISSN
1432-1440
Journal
Journal of Molecular Medicine
Quellenangaben
Volume: 88,
Issue: 8,
Pages: 745-752
Publisher
Springer
Non-patent literature
Publications
Reviewing status
Peer reviewed