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

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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 (US)
Pages (from-to)492-502
Number of pages11
JournalMucosal Immunology
Issue number2
StatePublished - Mar 1 2016

Bibliographical note

Funding Information:
We thank the Medical Research Council, the Wellcome Trust (086558, 102705, 97377) and the University of Aberdeen for funding. We thank Doreen Cantrell for useful comments, and acknowledge Medical Research Facility staff for care of the animals used in this study.

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