This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bobik, A. Articles by Kalinina, N. Search for Related Content PubMed PubMed Citation Articles by Bobik, A. Articles by Kalinina, N.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1873.)
© 2001 American Heart Association, Inc.

Editorials

Tumor Necrosis Factor Receptor and Ligand Superfamily Family Members TNFRSF14 and LIGHT

New Players in Human Atherogenesis

Alex Bobik; Natalia Kalinina

From the Baker Medical Research Institute and Alfred Hospital, Prahran, Victoria, Australia.

Correspondence to Dr Alex Bobik, Baker Medical Research Institute, Alfred Hospital, St Kilda Rd Central PO Box 6492, Melbourne, vic. 8008, Australia. E-mail alex.bobik@baker.edu.au

Increasing evidence indicates that atherosclerosis is the consequence of complex, multifactorial processes involving the abnormal interplay between local mechanisms involved in lipoprotein metabolism, the extracellular matrix and coagulation proteins, endothelial and smooth muscle cells, mononuclear leukocytes, and growth factors/cytokines.^1,2 A number of cytokines including those activating several members of the tumor necrosis factor (TNF) receptor superfamily have been consistently identified in atherosclerotic lesions and implicated in the pathogenesis of atherosclerosis. One of the earliest responses to hypercholesterolemia is an increase in the adherence of monocytes to arterial endothelium and then penetration into the intima. TNF- together with interleukin (IL)-1ß increases the adherence of leukocytes to endothelial cells,³ and in young ApoE-deficient mice, they promote monocyte accumulation within developing atherosclerotic lesions.⁴

See page 2004

In established lesions, the actions and patterns of expression of TNF receptor superfamily (TNFRSF) members and their activating ligands is complex and, in most cases, seems to lead to the development of complex atherosclerotic lesions that are susceptible to rupture. TNFRSF members are defined as those structurally related to the first family members TNFR1 and TNFR2, (now TNFRSF1A and TNFRSF1B, respectively).⁵ Each member contains multiple copies of a cysteine-rich motif of approximately 40 amino acids that is known to provide the ligand recognition motif; their cytoplasmic regions are frequently capable of stimulating the transcription factors activator protein-1 and nuclear factor-B. The latter factor is involved in regulating numerous genes critical for inflammatory responses, including IL-6, IL-8, vascular cell adhesion molecule-1, and E-selectin.⁶ A number of receptors . . . [Full Text of this Article]

This article has been cited by other articles:

				G. S. Getz Thematic review series: The Immune System and Atherogenesis. Immune function in atherogenesis J. Lipid Res., January 1, 2005; 46(1): 1 - 10. [Abstract] [Full Text] [PDF]

				T. Waehre, A. Yndestad, C. Smith, T. Haug, S. H. Tunheim, L. Gullestad, S. S. Froland, A. G. Semb, P. Aukrust, and J. K. Damas Increased Expression of Interleukin-1 in Coronary Artery Disease With Downregulatory Effects of HMG-CoA Reductase Inhibitors Circulation, April 27, 2004; 109(16): 1966 - 1972. [Abstract] [Full Text] [PDF]