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
Early online date	9 Sept 2015
DOIs	https://doi.org/10.1038/mi.2015.79
Publication status	Published - Mar 2016

Bibliographical note

ACKNOWLEDGMENTS
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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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.",

author = "Drummond, {R. A.} and Dambuza, {I. M.} and S. Vautier and Taylor, {J. A.} and Reid, {D. M.} and Bain, {C. C.} and Underhill, {D. M.} and D. Masopust and Kaplan, {D. H.} and Brown, {G. D.}",

note = "ACKNOWLEDGMENTS 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.",

year = "2016",

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doi = "10.1038/mi.2015.79",

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volume = "9",

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AU - Drummond, R. A.

AU - Dambuza, I. M.

AU - Vautier, S.

AU - Taylor, J. A.

AU - Reid, D. M.

AU - Bain, C. C.

AU - Underhill, D. M.

AU - Masopust, D.

AU - Kaplan, D. H.

AU - Brown, G. D.

N1 - ACKNOWLEDGMENTS 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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JO - Mucosal Immunology

JF - Mucosal Immunology

ER -

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

Abstract

Bibliographical note

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