Journal
JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 88, Issue 8, Pages 745-752Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00109-010-0631-4
Keywords
ITAM receptors; SYK; CARD9; Inflammasome; NLRP3; IL-1 beta
Funding
- Deutsche Krebshilfe
- DFG
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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-1 beta (IL-1 beta) 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-1 beta to initiate antifungal responses. Mature IL-1 beta production additionally requires cleavage of the pro-IL-1 beta 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-1 beta production in antifungal immunity.
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