Long-term activation of the innate immune system in atherosclerosis
Name:
Publisher version
View Source
Access full-text PDFOpen Access
View Source
Check access options
Check access options
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyDocument Type
Journal ArticlePublication Date
2016-08-01Keywords
AtherosclerosisChanged dietary components
Epigenetic reprogramming
Hyperlipidemia
Immuno-metabolism
Innate immune memory
Trained innate immunity
Cardiovascular Diseases
Immunity
Metadata
Show full item recordAbstract
Efforts to reverse the pathologic consequences of vulnerable plaques are often stymied by the complex treatment resistant pro-inflammatory environment within the plaque. This suggests that pro-atherogenic stimuli, such as LDL cholesterol and high fat diets may impart longer lived signals on (innate) immune cells that persist even after reversing the pro-atherogenic stimuli. Recently, a series of studies challenged the traditional immunological paradigm that innate immune cells cannot display memory characteristics. Epigenetic reprogramming in these myeloid cell subsets, after exposure to certain stimuli, has been shown to alter the expression of genes upon re-exposure. This phenomenon has been termed trained innate immunity or innate immune memory. The changed responses of 'trained' innate immune cells can confer nonspecific protection against secondary infections, suggesting that innate immune memory has likely evolved as an ancient mechanism to protect against pathogens. However, dysregulated processes of immunological imprinting mediated by trained innate immunity may also be detrimental under certain conditions as the resulting exaggerated immune responses could contribute to autoimmune and inflammatory diseases, such as atherosclerosis. Pro-atherogenic stimuli most likely cause epigenetic modifications that persist for prolonged time periods even after the initial stimulus has been removed. In this review we discuss the concept of trained innate immunity in the context of a hyperlipidemic environment and atherosclerosis. According to this idea the epigenome of myeloid (progenitor) cells is presumably modified for prolonged periods of time, which, in turn, could evoke a condition of continuous immune cell over-activation. reserved.Source
Semin Immunol. 2016 Aug;28(4):384-93. doi: 10.1016/j.smim.2016.04.004. Epub 2016 Apr 22. Link to article on publisher's siteDOI
10.1016/j.smim.2016.04.004Permanent Link to this Item
http://hdl.handle.net/20.500.14038/40054PubMed ID
27113267Related Resources
Link to Article in PubMedRights
Open Access funded by VSNU. Under a Creative Commons license, http://creativecommons.org/licenses/by/4.0/.
Distribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.1016/j.smim.2016.04.004
Scopus Count
Collections
Except where otherwise noted, this item's license is described as <p>Open Access funded by VSNU. Under a Creative Commons license, http://creativecommons.org/licenses/by/4.0/.</p>