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.