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Poeck, H.* ; Ruland, J.

SYK kinase signaling and the NLRP3 inflammasome in antifungal immunity.

J. Mol. Med. 88, 745-752 (2010)
Verlagsversion DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter ITAM receptors; SYK; CARD9; Inflammasome; NLRP3; IL-1β
ISSN (print) / ISBN 0946-2716
e-ISSN 1432-1440
Zeitschrift Journal of Molecular Medicine
Quellenangaben Band: 88, Heft: 8, Seiten: 745-752 Artikelnummer: , Supplement: ,
Verlag Springer
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOXI)