Journal of Clinical Immunology

, Volume 30, Issue 4, pp 496–501

ITAM Receptor Signaling and the NLRP3 Inflammasome in Antifungal Immunity

Article

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

Abstract

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-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.

Scope

Here, we discuss how ITAM receptor signaling and NLRP3 cooperate for the induction of antifungal immunity.

Keywords

ITAM receptors SYK CARD9 inflammasome NLRP3 IL-1β 

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.III. Medizinische Klinik, Klinikum rechts der IsarTechnische Universität MünchenMunichGermany
  2. 2.Laboratory of Signaling in the Immune System, Helmholtz Zentrum MünchenGerman Research Center for Environmental HealthNeuherbergGermany

Personalised recommendations