CD137: A checkpoint regulator involved in atherosclerosis

Atherosclerosis. 2018 May:272:66-72. doi: 10.1016/j.atherosclerosis.2018.03.007. Epub 2018 Mar 5.

Abstract

Inflammation is associated with atherosclerotic plaque development and precipitation of myocardial infarction and stroke, and anti-inflammatory therapy may reduce disease severity. Costimulatory molecules are key regulators of immune cell activity and inflammation, and are associated with disease development in atherosclerosis. Accumulating evidence indicates that a costimulatory molecule of the Tumor Necrosis Factor Receptor superfamily, the checkpoint regulator CD137, promotes atherosclerosis and vascular inflammation in experimental models. In light of the burgeoning consideration of CD137-targeted therapy in the clinic, it will be important to better understand costimulator immunobiology in development of cardiovascular disease. Here, we review available data on the costimulator CD137 and its potential role in atherosclerosis.

Keywords: 4-1BB; Cardiovascular disease; Costimulation; Inflammation; Leukocytes; Tumor necrosis factor receptor superfamily; Vascular inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Apolipoproteins E / metabolism
  • Atherosclerosis / metabolism*
  • Humans
  • Immune System
  • Inflammation
  • Lymphocyte Activation
  • Plaque, Atherosclerotic / metabolism
  • Signal Transduction
  • T-Lymphocytes / cytology*
  • Tumor Necrosis Factor Receptor Superfamily, Member 9 / metabolism*

Substances

  • Anti-Inflammatory Agents
  • Apolipoproteins E
  • TNFRSF9 protein, human
  • Tumor Necrosis Factor Receptor Superfamily, Member 9