Functions and regulation of T cell-derived interleukin-10.
Allergy
Autoimmune disease
Blimp-1
GWAS
Human
IL-10
Infection
Inflammatory bowel disease
Intestinal homeostasis
Regulatory T cell
T cell
Transcriptional regulation
Tumor
c-Maf
Journal
Seminars in immunology
ISSN: 1096-3618
Titre abrégé: Semin Immunol
Pays: England
ID NLM: 9009458
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
13
10
2019
accepted:
28
10
2019
pubmed:
16
11
2019
medline:
22
5
2020
entrez:
16
11
2019
Statut:
ppublish
Résumé
Interleukin (IL)-10 is an essential anti-inflammatory cytokine and functions as a negative regulator of immune responses to microbial antigens. IL-10 is particularly important in maintaining the intestinal microbe-immune homeostasis. Loss of IL-10 promotes the development of inflammatory bowel disease (IBD) as a consequence of an excessive immune response to the gut microbiota. IL-10 also functions more generally to prevent excessive inflammation during the course of infection. Although IL-10 can be produced by virtually all cells of the innate and adaptive immune system, T cells constitute a non-redundant source for IL-10 in many cases. The various roles of T cell-derived IL-10 will be discussed in this review. Given that IL-10 is at the center of maintaining the delicate balance between effective immunity and tissue protection, it is not surprising that IL-10 expression is highly dynamic and tightly regulated. We summarize the environmental signals and molecular pathways that regulate IL-10 expression. While numerous studies have provided us with a deep understanding of IL-10 biology, the majority of findings have been made in murine models, prompting us to highlight gaps in our knowledge about T cell-derived IL-10 in the human system.
Identifiants
pubmed: 31727465
pii: S1044-5323(19)30080-6
doi: 10.1016/j.smim.2019.101344
pii:
doi:
Substances chimiques
Interleukin-10
130068-27-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
101344Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.