Human Anti-fungal Th17 Immunity and Pathology Rely on Cross-Reactivity against Candida albicans.
Aspergillus fumigatus
Candida albicans
T cell cross-reactivity
Th17
airway inflammation
allergic bronchopulmonary aspergillosis (ABPA)
anti-fungal immunity
antigen-reactive T cell enrichment (ARTE)
cystic fibrosis
heterologous immunity
microbiota
Journal
Cell
ISSN: 1097-4172
Titre abrégé: Cell
Pays: United States
ID NLM: 0413066
Informations de publication
Date de publication:
07 03 2019
07 03 2019
Historique:
received:
17
07
2018
revised:
06
11
2018
accepted:
24
01
2019
pubmed:
26
2
2019
medline:
7
1
2020
entrez:
26
2
2019
Statut:
ppublish
Résumé
Th17 cells provide protection at barrier tissues but may also contribute to immune pathology. The relevance and induction mechanisms of pathologic Th17 responses in humans are poorly understood. Here, we identify the mucocutaneous pathobiont Candida albicans as the major direct inducer of human anti-fungal Th17 cells. Th17 cells directed against other fungi are induced by cross-reactivity to C. albicans. Intestinal inflammation expands total C. albicans and cross-reactive Th17 cells. Strikingly, Th17 cells cross-reactive to the airborne fungus Aspergillus fumigatus are selectively activated and expanded in patients with airway inflammation, especially during acute allergic bronchopulmonary aspergillosis. This indicates a direct link between protective intestinal Th17 responses against C. albicans and lung inflammation caused by airborne fungi. We identify heterologous immunity to a single, ubiquitous member of the microbiota as a central mechanism for systemic induction of human anti-fungal Th17 responses and as a potential risk factor for pulmonary inflammatory diseases.
Identifiants
pubmed: 30799037
pii: S0092-8674(19)30104-7
doi: 10.1016/j.cell.2019.01.041
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1340-1355.e15Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.