INTRODUCTION: 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.