Dendritic cell-derived TGF-β mediates the induction of mucosal regulatory T-cell response to Helicobacter infection essential for maintenance of immune tolerance in mice.
helicobacter felis
gastroenterology
immune response
Journal
Helicobacter
ISSN: 1523-5378
Titre abrégé: Helicobacter
Pays: England
ID NLM: 9605411
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
received:
21
07
2020
revised:
04
09
2020
accepted:
15
09
2020
pubmed:
8
10
2020
medline:
15
9
2021
entrez:
7
10
2020
Statut:
ppublish
Résumé
Helicobacter pylori infection leads to regulatory T-cell (Treg) induction in infected mice, which contributes to H. pylori immune escape. However, the mechanisms responsible for H. pylori induction of Treg and immune tolerance remain unclear. We hypothesized DC-produced TGF-β may be responsible for Treg induction and immune tolerance. To test this hypothesis, we generated TGF-β When stimulated with H. pylori, TGF-β Our findings indicate that DC-derived TGF-β mediates Helicobacter-induced Treg response and attenuates the inflammatory Th1 response. We also demonstrated a previously unrecognized innate role of DC controlling Helicobacter colonization via a Treg-independent mechanism. DC TGF-β signaling may represent an important target in the management of H. pylori.
Sections du résumé
BACKGROUND
BACKGROUND
Helicobacter pylori infection leads to regulatory T-cell (Treg) induction in infected mice, which contributes to H. pylori immune escape. However, the mechanisms responsible for H. pylori induction of Treg and immune tolerance remain unclear. We hypothesized DC-produced TGF-β may be responsible for Treg induction and immune tolerance.
MATERIALS AND METHODS
METHODS
To test this hypothesis, we generated TGF-β
RESULTS
RESULTS
When stimulated with H. pylori, TGF-β
CONCLUSIONS
CONCLUSIONS
Our findings indicate that DC-derived TGF-β mediates Helicobacter-induced Treg response and attenuates the inflammatory Th1 response. We also demonstrated a previously unrecognized innate role of DC controlling Helicobacter colonization via a Treg-independent mechanism. DC TGF-β signaling may represent an important target in the management of H. pylori.
Identifiants
pubmed: 33025641
doi: 10.1111/hel.12763
pmc: PMC7885176
mid: NIHMS1667103
doi:
Substances chimiques
Transforming Growth Factor beta
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12763Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK087708-01
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI154128
Pays : United States
Organisme : NIDDK NIH HHS
ID : NIH P30-DK034933-35
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK034933
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK087708
Pays : United States
Informations de copyright
© 2020 John Wiley & Sons Ltd.
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