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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.

journal_name

Mucosal Immunol

journal_title

Mucosal immunology

authors

Drummond RA,Dambuza IM,Vautier S,Taylor JA,Reid DM,Bain CC,Underhill DM,Masopust D,Kaplan DH,Brown GD

doi

10.1038/mi.2015.79

subject

Has Abstract

pub_date

2016-03-01 00:00:00

pages

492-502

issue

2

eissn

1933-0219

issn

1935-3456

pii

mi201579

journal_volume

9

pub_type

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