CD4+ T-cell survival in the GI tract requires dectin-1 during fungal infection

Research output: Contribution to journalArticlepeer-review


  • I. M. Dambuza
  • S. Vautier
  • J. A. Taylor
  • D. M. Reid
  • C. C. Bain
  • D. M. Underhill
  • D. Masopust
  • D. H. Kaplan
  • G. D. Brown

Colleges, School and Institutes

External organisations

  • Institute of Medical Sciences
  • National Institute of Health
  • University of Glasgow
  • Cedars-Sinai Medical Centre
  • University of Minnesota Medical School
  • University of Minnesota Twin Cities


Dectin-1 is an innate antifungal C-type lectin receptor necessary for protective antifungal immunity. We recently discovered that Dectin-1 is involved in controlling fungal infections of the gastrointestinal (GI) tract, but how this C-type lectin receptor mediates these activities is unknown. Here, we show that Dectin-1 is essential for driving fungal-specific CD4+ T-cell responses in the GI tract. Loss of Dectin-1 resulted in abrogated dendritic cell responses in the mesenteric lymph nodes (mLNs) and defective T-cell co-stimulation, causing substantial increases in CD4+ T-cell apoptosis and reductions in the cellularity of GI-associated lymphoid tissues. CD8+ T-cell responses were unaffected by Dectin-1 deficiency. These functions of Dectin-1 have significant implications for our understanding of intestinal immunity and susceptibility to fungal infections.


Original languageEnglish
Pages (from-to)492-502
Number of pages11
JournalMucosal immunology
Issue number2
Early online date9 Sep 2015
Publication statusPublished - 1 Mar 2016

ASJC Scopus subject areas