Influence of CD4+/CD25+ regulatory T cells on atherogenesis in patients with end-stage kidney disease.

Details

Serval ID
serval:BIB_D2AADB437C25
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Influence of CD4+/CD25+ regulatory T cells on atherogenesis in patients with end-stage kidney disease.
Journal
Expert Review of Cardiovascular Therapy
Author(s)
Meier P., Meier R., Blanc E.
ISSN
1477-9072
Publication state
Published
Issued date
2008
Volume
6
Number
7
Pages
987-997
Language
english
Notes
Publication types: Journal Article ; Review
Abstract
Atherosclerosis, which is influenced by both traditional and nontraditional cardiovascular risk factors and has been characterized as an inflammatory process, is considered to be the main cause of the elevated cardiovascular risk associated with chronic kidney disease. The inflammatory component of atherosclerosis can be separated into an innate immune response involving monocytes and macrophages that respond to the excessive uptake of lipoproteins and an adaptive immune response that involves antigen-specific T cells. Concurrent with the influx of immune cells to the site of atherosclerotic lesion, the role of the adaptive immune response gradually increases. One of those cells are represented by the CD4+/CD25+ Tregs, which play indispensable roles in the maintenance of natural self-tolerance and negative control of pathological, as well as physiological, immune responses. Altered self-antigens such as oxidized LDLs may induce the development of CD4+/CD25+ Tregs with atheroprotective properties. However, atherosclerosis may be promoted by an imbalance between regulatory and pathogenic immunity that may be represented by the low expression of the forkhead box transcription factor (Foxp3) in CD4+/CD25+ Tregs. Such a defect may break immunologic tolerance and alter both specific and bystander immune suppression, leading to exacerbation of plaque development. Patients with end-stage kidney disease (ESKD) display a cellular immune dysfunction and accelerated atherosclerosis. Uremic solutes that accumulate during ESKD may be involved in these processes. In patients with ESKD and especially in those that are chronically hemodialyzed, oxidative stress induced by oxidized LDLs may increase CD4+/CD25+ Treg sensitivity to Fas-mediated apoptosis as a consequence of specific dysregulation of IL-2 expression. This review will focus on the current state of knowledge regarding the influence of CD4+/CD25+ Tregs on atherogenesis in patients with ESKD, and the potential effect of statins on the circulating number and the functional properties of these cells.
Keywords
Animals, Antigens, CD24, Atherosclerosis/complications, Atherosclerosis/etiology, Cardiovascular Diseases/etiology, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology, Interleukin-2 Receptor alpha Subunit, Kidney Failure, Chronic/complications, Kidney Failure, Chronic/immunology, Risk Factors, T-Lymphocytes, Regulatory/drug effects, T-Lymphocytes, Regulatory/immunology
Pubmed
Create date
12/10/2009 12:52
Last modification date
20/08/2019 15:52
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