Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand

Although the majority of research on CD137 has been directed to T cells, it is becoming clear that this molecule has distinct functions in other lineages of cells, including non-hematopoietic cells. In particular, emerging evidence suggests that the CD137-its ligand (CD137L) network involving immune...

Full description

Bibliographic Details
Main Author: Kwon, Byungsuk
Format: Online
Language:English
Published: The Korean Association of Immunologists 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509161/
id pubmed-3509161
recordtype oai_dc
spelling pubmed-35091612012-12-04 Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand Kwon, Byungsuk Review Article Although the majority of research on CD137 has been directed to T cells, it is becoming clear that this molecule has distinct functions in other lineages of cells, including non-hematopoietic cells. In particular, emerging evidence suggests that the CD137-its ligand (CD137L) network involving immune cells and non-immune cells, directly or indirectly regulates inflammation in both positive and negative manners. Bidirectional signaling through both CD137 and CD137L is critical in the evolution of inflammation: 1) CD137L signaling plays an indispensible role in the activation and recruitment of neutrophils by inducing the production of proinflammatory cytokines and chemokines in hematopoietic and non-hematopoietic cells such as macrophages, endothelial cells and epithelial cells; 2) CD137 signaling in NK cells and T cells is required for their activation and can influence other cells participating in inflammation via either their production of proinflammatory cytokines or engagement of CD137L by their cell surface CD137: 3) CD137 signaling can suppress inflammation by controlling regulatory activities of dendritic cells and regulatory T cells. As recognition grows of the role of dysregulated CD137 or CD137L stimulation in inflammatory diseases, significant efforts will be needed to develop antagonists to CD137 or CD137L. The Korean Association of Immunologists 2012-10 2012-10-31 /pmc/articles/PMC3509161/ /pubmed/23213310 http://dx.doi.org/10.4110/in.2012.12.5.176 Text en Copyright © 2012 The Korean Association of Immunologists http://creativecommons.org/licenses/by-nc/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Kwon, Byungsuk
spellingShingle Kwon, Byungsuk
Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
author_facet Kwon, Byungsuk
author_sort Kwon, Byungsuk
title Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
title_short Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
title_full Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
title_fullStr Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
title_full_unstemmed Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand
title_sort regulation of inflammation by bidirectional signaling through cd137 and its ligand
description Although the majority of research on CD137 has been directed to T cells, it is becoming clear that this molecule has distinct functions in other lineages of cells, including non-hematopoietic cells. In particular, emerging evidence suggests that the CD137-its ligand (CD137L) network involving immune cells and non-immune cells, directly or indirectly regulates inflammation in both positive and negative manners. Bidirectional signaling through both CD137 and CD137L is critical in the evolution of inflammation: 1) CD137L signaling plays an indispensible role in the activation and recruitment of neutrophils by inducing the production of proinflammatory cytokines and chemokines in hematopoietic and non-hematopoietic cells such as macrophages, endothelial cells and epithelial cells; 2) CD137 signaling in NK cells and T cells is required for their activation and can influence other cells participating in inflammation via either their production of proinflammatory cytokines or engagement of CD137L by their cell surface CD137: 3) CD137 signaling can suppress inflammation by controlling regulatory activities of dendritic cells and regulatory T cells. As recognition grows of the role of dysregulated CD137 or CD137L stimulation in inflammatory diseases, significant efforts will be needed to develop antagonists to CD137 or CD137L.
publisher The Korean Association of Immunologists
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509161/
_version_ 1611936299463213056