CD4
CP: Immunology
CP: Neuroscience
T cells
autoimmunity
cell death
experimental autoimmune encephalomyelitis, EAE
inflammation
interleukin-10
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
29 03 2022
29 03 2022
Historique:
received:
20
04
2021
revised:
05
01
2022
accepted:
03
03
2022
entrez:
30
3
2022
pubmed:
31
3
2022
medline:
2
4
2022
Statut:
ppublish
Résumé
Interleukin (IL)-10 is considered a prototypical anti-inflammatory cytokine, significantly contributing to the maintenance and reestablishment of immune homeostasis. Accordingly, it has been shown in the intestine that IL-10 produced by Tregs can act on effector T cells, thereby limiting inflammation. Herein, we investigate whether this role also applies to IL-10 produced by T cells during central nervous system (CNS) inflammation. During neuroinflammation, both CNS-resident and -infiltrating cells produce IL-10; yet, as IL-10 has a pleotropic function, the exact contribution of the different cellular sources is not fully understood. We find that T-cell-derived IL-10, but not other relevant IL-10 sources, can promote inflammation in experimental autoimmune encephalomyelitis. Furthermore, in the CNS, T-cell-derived IL-10 acts on effector T cells, promoting their survival and thereby enhancing inflammation and CNS autoimmunity. Our data indicate a pro-inflammatory role of T-cell-derived IL-10 in the CNS.
Identifiants
pubmed: 35354043
pii: S2211-1247(22)00309-6
doi: 10.1016/j.celrep.2022.110565
pii:
doi:
Substances chimiques
IL10 protein, mouse
0
Interleukin-10
130068-27-8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110565Subventions
Organisme : Wellcome Trust
ID : 102972
Pays : United Kingdom
Informations de copyright
Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no conflicts of interest.