Role of osteopontin in dendritic cell shaping of immune responses.
Autoimmune diseases
Cancer
Dendritic cells
Mesenchymal stromal cells
Osteopontin
T cell polarization
Journal
Cytokine & growth factor reviews
ISSN: 1879-0305
Titre abrégé: Cytokine Growth Factor Rev
Pays: England
ID NLM: 9612306
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
15
04
2019
accepted:
09
05
2019
pubmed:
28
5
2019
medline:
24
7
2020
entrez:
26
5
2019
Statut:
ppublish
Résumé
Osteopontin (OPN) is a pleiotropic cytokine produced both by immune and non-immune cells and active on different cellular targets. OPN production has been associated with several pathological conditions, including autoimmune diseases (e.g. lupus, multiple sclerosis and rheumatoid arthritis) and cancer. Emerging evidence suggests that the role of OPN has been underestimated, as it seems to be working at multiple levels of immune regulation, such as the shaping of T cell effector responses, the regulation of the tumor microenvironment, and the functional interaction with mesenchymal stromal cells. In this context, dendritic cells (DCs) play a crucial role being both an important source and a cellular target for OPN action. DC family is composed by several cell subsets endowed with specific immune functions. OPN exerts its biological functions through multiple receptors and is produced in different intracellular and secreted forms. OPN production by DC subsets is emerging as a crucial mechanism of regulation in normal and pathological conditions and starts to be exploited as a therapeutic target. This review will focus on the role of DC-derived OPN in shaping immune response and on the complex role of this cytokines in the regulation in immune response.
Identifiants
pubmed: 31126876
pii: S1359-6101(19)30054-1
doi: 10.1016/j.cytogfr.2019.05.004
pii:
doi:
Substances chimiques
Cytokines
0
Osteopontin
106441-73-0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
19-28Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.