Journal of Clinical Immunology

, Volume 30, Issue 4, pp 496-501

First online:

ITAM Receptor Signaling and the NLRP3 Inflammasome in Antifungal Immunity

  • Hendrik PoeckAffiliated withIII. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München
  • , Jürgen RulandAffiliated withIII. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität MünchenLaboratory of Signaling in the Immune System, Helmholtz Zentrum München, German Research Center for Environmental Health Email author 

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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-1β to initiate antifungal responses. Mature IL-1β production requires in addition to the synthesis of pro-IL-1β 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.


ITAM receptors SYK CARD9 inflammasome NLRP3 IL-1β