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

doi:10.1038/mi.2015.79

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

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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.

Original language	English
Pages (from-to)	492-502
Number of pages	11
Journal	Mucosal Immunology
Volume	9
Issue number	2
Early online date	9 Sept 2015
DOIs	https://doi.org/10.1038/mi.2015.79
Publication status	Published - 1 Mar 2016
Externally published	Yes

Bibliographical note

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Copyright © and Moral Rights are retained by the author(s) and/ or other copyright owners. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This item cannot be reproduced or quoted extensively from without first obtaining permission in writing from the copyright holder(s). The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the copyright holders.

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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Cite this

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

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.",

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