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

R. A. Drummond, 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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)


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 Sept 2015
Publication statusPublished - 1 Mar 2016

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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