HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Lymphocytic tumor necrosis factor receptor superfamily co-stimulatory molecules in the pathogenesis of atherosclerosis.

AbstractPURPOSE OF REVIEW:
The role of lymphocytes in the chronic inflammatory disease atherosclerosis has emerged over the past decade. Co-stimulatory molecules of the heterogeneous tumor necrosis factor receptor superfamily play a pivotal role in lymphocyte activation, proliferation and differentiation. Here we describe the immune modulatory properties and mechanisms of four tumor necrosis factor receptor superfamily members in atherosclerosis.
RECENT FINDINGS:
CD40/CD40L, OX40L/OX40, CD70/CD27 and CD137/CD137L are present in human atherosclerotic plaques and have shown strong immune modulatory functions in atherosclerosis, resulting in either atherogenic or atheroprotective effects in mouse models of atherosclerosis.
SUMMARY:
Insight into the immune modulatory mechanisms of co-stimulatory interactions in atherosclerosis can contribute to clinical exploitation of these interactions in the treatment of cardiovascular disease.
AuthorsEsther Smeets, Svenja Meiler, Esther Lutgens
JournalCurrent opinion in lipidology (Curr Opin Lipidol) Vol. 24 Issue 6 Pg. 518-24 (Dec 2013) ISSN: 1473-6535 [Electronic] England
PMID24184937 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Receptors, Tumor Necrosis Factor
Topics
  • Animals
  • Atherosclerosis (etiology, metabolism)
  • Humans
  • Lymphocytes (metabolism)
  • Receptors, Tumor Necrosis Factor (metabolism)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: