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Poeck, H.* ; Ruland, J.

ITAM receptor signaling and the NLRP3 inflammasome in antifungal immunity.

J. Clin. Immunol. 30, 496-501 (2010)
Verlagsversion DOI PMC
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter ITAM receptors; SYK; CARD9; inflammasome; NLRP3; IL-1 beta
ISSN (print) / ISBN 0271-9142
e-ISSN 1573-2592
Zeitschrift Journal of Clinical Immunology
Quellenangaben Band: 30, Heft: 4, Seiten: 496-501 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort New York, NY
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOXI)