CD4+ T-cell survival in the GI tract requires dectin-1 during fungal infection
Research output: Contribution to journal › Article › peer-review
Authors
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
Abstract
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.
Details
Original language | English |
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Pages (from-to) | 492-502 |
Number of pages | 11 |
Journal | Mucosal immunology |
Volume | 9 |
Issue number | 2 |
Early online date | 9 Sep 2015 |
Publication status | Published - 1 Mar 2016 |