CD4(+) T-cell survival in the GI tract requires dectin-1 during fungal infection.
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.
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
R A
RA
Drummond
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
I M
IM
Dambuza
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
S
S
Vautier
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
J A
JA
Taylor
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
D M
DM
Reid
Institute of Infection, Immunity and Inflammation, College of Veterinary, Medical and Life Science, University of Glasgow, Scotland, UK.
C C
CC
Bain
Division of Immunology, The Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Centre, Los Angeles, California, USA.
D M
DM
Underhill
Department of Microbiology, Centre for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
D
D
Masopust
Department of Dermatology, Centre for Immunology, University of Minnesota, Minneapolis, Minnesota, USA.
D H
DH
Kaplan
Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
G D
GD
Brown
D019264:Adoptive Transfer; D000818:Animals; D017209:Apoptosis / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000382:microbiology / Q000473:pathology / Q000637:transplantation; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D002176:Candida albicans / Q000276:immunology*; D002177:Candidiasis / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D002470:Cell Survival / Q000276:immunology; D005260:Female; D041981:Gastrointestinal Tract / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D015870:Gene Expression; D037181:Lectins, C-Type / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D008198:Lymph Nodes / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D008213:Lymphocyte Activation; D008643:Mesentery / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D000099181:Dectin-1
D037181:Lectins, C-Type; D000099181:Dectin-1