Autophagic induction modulates splenic plasmacytoid dendritic cell mediated immune response in cerebral malarial infection model.
Animals
Autophagy
/ drug effects
CD8-Positive T-Lymphocytes
/ immunology
Cell Adhesion
/ drug effects
Cytokines
/ immunology
Dendritic Cells
/ immunology
Disease Models, Animal
Malaria, Cerebral
/ drug therapy
Male
Mice
Sirolimus
/ administration & dosage
Spleen
/ immunology
T-Lymphocytes, Regulatory
/ immunology
Th1-Th2 Balance
/ drug effects
Th17 Cells
/ immunology
Autophagy
Cerebral malaria
Plasmodium berghei
Th1-Th2 immune response
mDC-pDC ratio
pDC-antigen presentation
Journal
Microbes and infection
ISSN: 1769-714X
Titre abrégé: Microbes Infect
Pays: France
ID NLM: 100883508
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
12
12
2018
revised:
16
05
2019
accepted:
28
05
2019
pubmed:
12
6
2019
medline:
28
12
2019
entrez:
12
6
2019
Statut:
ppublish
Résumé
Splenic plasmacytoid dendritic cells (pDC) possess the capability to harbor live replicative Plasmodium parasite. Isolated splenic pDC from infected mice causes malaria when transferred to naïve mice. Incomplete autophagic degradation might cause poor antigen processing and poor immune response. Induction of autophagic flux by rapamycin treatment led to better prognosis by boosting pDC centered immune response against the pathogen. Splenic pDC from rapamycin-treated infected mice, caused less parasitemia in naïve mice. The downregulation of adhesion with unaltered phagocytic potential of the cells post autophagic induction restricted excessive parasite burden within them. Rapamycin-treated pDC played a better role in antigen presentation. They showed higher expression of co-stimulatory molecules CD80, CD86, DEC205, MHCI. Rapamycin-treated pDC induced CD28 expression on CD8
Identifiants
pubmed: 31185303
pii: S1286-4579(19)30060-7
doi: 10.1016/j.micinf.2019.05.004
pii:
doi:
Substances chimiques
Cytokines
0
Sirolimus
W36ZG6FT64
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
475-484Informations de copyright
Copyright © 2019 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.