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Updated: Jun 13, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
ITAM receptor signaling and the NLRP3 inflammasome in antifungal immunity
1III. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, 81675, Munich, Germany.
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.
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