ITAM receptor signaling and the NLRP3 inflammasome in antifungal immunity

Hendrik Poeck, Jürgen Ruland

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations

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.

Original languageEnglish
Pages (from-to)496-501
Number of pages6
JournalJournal of Clinical Immunology
Volume30
Issue number4
DOIs
StatePublished - Jul 2010
Externally publishedYes

Keywords

  • CARD9
  • IL-1β
  • ITAM receptors
  • Inflammasome
  • NLRP3
  • SYK

Fingerprint

Dive into the research topics of 'ITAM receptor signaling and the NLRP3 inflammasome in antifungal immunity'. Together they form a unique fingerprint.

Cite this