A Subset of Type I Conventional Dendritic Cells Controls Cutaneous Bacterial Infections through VEGFα-Mediated Recruitment of Neutrophils.
Acne Vulgaris
/ immunology
Animals
Antigen Presentation
Chemotaxis, Leukocyte
/ immunology
Dendritic Cells
/ classification
Ear, External
Gene Expression Regulation
Gene Ontology
Gram-Positive Bacterial Infections
/ immunology
Humans
Injections, Intradermal
Mice
Mice, Inbred C57BL
Neutrophil Infiltration
/ immunology
Neutrophils
/ metabolism
Propionibacterium acnes
RNA, Messenger
/ biosynthesis
Single-Cell Analysis
Vascular Endothelial Growth Factor A
/ biosynthesis
VEGF
VEGFR
XCR1
activation
cDC1
dendritic cell
langerin
monocyte
neutrophil
recruitment
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
16 04 2019
16 04 2019
Historique:
received:
09
03
2018
revised:
14
11
2018
accepted:
27
02
2019
pubmed:
31
3
2019
medline:
17
9
2019
entrez:
31
3
2019
Statut:
ppublish
Résumé
Skin conventional dendritic cells (cDCs) exist as two distinct subsets, cDC1s and cDC2s, which maintain the balance of immunity to pathogens and tolerance to self and microbiota. Here, we examined the roles of dermal cDC1s and cDC2s during bacterial infection, notably Propionibacterium acnes (P. acnes). cDC1s, but not cDC2s, regulated the magnitude of the immune response to P. acnes in the murine dermis by controlling neutrophil recruitment to the inflamed site and survival and function therein. Single-cell mRNA sequencing revealed that this regulation relied on secretion of the cytokine vascular endothelial growth factor α (VEGF-α) by a minor subset of activated EpCAM
Identifiants
pubmed: 30926233
pii: S1074-7613(19)30091-3
doi: 10.1016/j.immuni.2019.03.001
pii:
doi:
Substances chimiques
RNA, Messenger
0
VEGFA protein, human
0
Vascular Endothelial Growth Factor A
0
vascular endothelial growth factor A, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Video-Audio Media
Langues
eng
Sous-ensembles de citation
IM
Pagination
1069-1083.e8Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.