Journal of Clinical Immunology

, Volume 30, Issue 4, pp 496–501

ITAM Receptor Signaling and the NLRP3 Inflammasome in Antifungal Immunity


  • Hendrik Poeck
    • III. Medizinische Klinik, Klinikum rechts der IsarTechnische Universität München
    • III. Medizinische Klinik, Klinikum rechts der IsarTechnische Universität München
    • Laboratory of Signaling in the Immune System, Helmholtz Zentrum MünchenGerman Research Center for Environmental Health

DOI: 10.1007/s10875-010-9385-6

Cite this article as:
Poeck, H. & Ruland, J. J Clin Immunol (2010) 30: 496. doi:10.1007/s10875-010-9385-6



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 receptorsSYKCARD9inflammasomeNLRP3IL-1β

Copyright information

© Springer Science+Business Media, LLC 2010