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dc.contributor.authorChrist, Anette
dc.contributor.authorBekkering, Siroon
dc.contributor.authorLatz, Eicke
dc.contributor.authorRiksen, Niels P.
dc.date2022-08-11T08:09:45.000
dc.date.accessioned2022-08-23T16:42:15Z
dc.date.available2022-08-23T16:42:15Z
dc.date.issued2016-08-01
dc.date.submitted2016-08-16
dc.identifier.citationSemin Immunol. 2016 Aug;28(4):384-93. doi: 10.1016/j.smim.2016.04.004. Epub 2016 Apr 22. <a href="http://dx.doi.org/10.1016/j.smim.2016.04.004">Link to article on publisher's site</a>
dc.identifier.issn1044-5323 (Linking)
dc.identifier.doi10.1016/j.smim.2016.04.004
dc.identifier.pmid27113267
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40054
dc.description.abstractEfforts 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27113267&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Open Access funded by VSNU. Under a Creative Commons license, http://creativecommons.org/licenses/by/4.0/.</p>
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAtherosclerosis
dc.subjectChanged dietary components
dc.subjectEpigenetic reprogramming
dc.subjectHyperlipidemia
dc.subjectImmuno-metabolism
dc.subjectInnate immune memory
dc.subjectTrained innate immunity
dc.subjectCardiovascular Diseases
dc.subjectImmunity
dc.titleLong-term activation of the innate immune system in atherosclerosis
dc.typeJournal Article
dc.source.journaltitleSeminars in immunology
dc.source.volume28
dc.source.issue4
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3864&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2859
dc.identifier.contextkey8985411
refterms.dateFOA2022-08-23T16:42:15Z
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/2859
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages384-93


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<p>Open Access funded by VSNU. Under a Creative Commons license, http://creativecommons.org/licenses/by/4.0/.</p>
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>