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Gerdes, N; Zirlik, A.
Co-stimulatory molecules in and beyond co-stimulation - tipping the balance in atherosclerosis?
THROMB HAEMOSTASIS. 2011; 106(5): 804-813. Doi: 10.1160/TH11-09-0605
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Co-Autor*innen der Med Uni Graz
Zirlik Andreas
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Abstract:
A plethora of basic laboratory and clinical studies has uncovered the chronic inflammatory nature of atherosclerosis. The adaptive immune system with its front-runner, the T cell, drives the atherogenic process at all stages. T cell function is dependent on and controlled by a variety of either co-stimulatory or co-inhibitory signals. In addition, many of these proteins enfold T cell-independent pro-atherogenic functions on a variety of cell types. Accordingly they represent potential targets for immune-modulatory and/or anti-inflammatory therapy of atherosclerosis. This review focuses on the diverse role of co-stimulatory molecules of the B7 and tumour necrosis factor (TNF)-superfamily and their downstream signalling effectors in atherosclerosis. In particular, the contribution of CD28/CD80/CD86/CTLA4, ICOS/ICOSL, PD-1/PDL-1/2, TRAF, CD40/CD154, OX40/OX40L, CD137/CD137L, CD70/CD27, GITR/GITRL, and LIGHT to arterial disease is reviewed. Finally, the potential for a therapeutic exploitation of these molecules in the treatment of atherosclerosis is discussed.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Arteries - immunology
Atherosclerosis - immunology
Atherosclerosis - therapy
B7 Antigens - metabolism
Costimulatory and Inhibitory T-Cell Receptors - metabolism
Humans -
Immunotherapy - methods
Inflammation - immunology
Inflammation - therapy
Inflammation Mediators - metabolism
Lymphocyte Activation -
Receptors, Tumor Necrosis Factor - metabolism
Signal Transduction -
T-Lymphocytes - immunology

Find related publications in this database (Keywords)
Animal models
atherosclerosis
leukocyte function / activation
inflammatory mediators
immunity
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