Regulation of Inflammation by Bidirectional Signaling through CD137 and Its Ligand.
- Author:
Byungsuk KWON
1
Author Information
- Publication Type:Review
- Keywords: CD137; CD137L; Inflammation
- MeSH: Chemokines; Cytokines; Dendritic Cells; Endothelial Cells; Inflammation; Killer Cells, Natural; Macrophages; Neutrophils; T-Lymphocytes; T-Lymphocytes, Regulatory
- From:Immune Network 2012;12(5):176-180
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
