Journal
JOURNAL OF CLINICAL IMMUNOLOGY
Volume 30, Issue 4, Pages 496-501Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-010-9385-6
Keywords
ITAM receptors; SYK; CARD9; inflammasome; NLRP3; IL-1 beta
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Funding
- Deutsche Krebshilfe
- DFG
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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-1 beta to initiate antifungal responses. Mature IL-1 beta production requires in addition to the synthesis of pro-IL-1 beta a cleavage of the precursor protein by the inflammatory Caspase-1 which is controlled within the NLRP3 inflammasome. Here, we discuss how ITAM receptor signaling and NLRP3 cooperate for the induction of antifungal immunity.
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