| Epigenetic regulation of immune cell functions during post-septic immunosuppression. | |
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MedLine Citation:
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PMID: 21048427 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Studies in humans and animal models indicate that profound immunosuppression is one of the chronic consequences of severe sepsis. This immune dysfunction encompasses deficiencies in activation of cells in both the myeloid and lymphoid cell lineages. As a result, survivors of severe sepsis are at risk of succumbing to infections perpetrated by opportunistic pathogens that are normally controlled by a fully functioning immune system. Recent studies have indicated that epigenetic mechanisms may be one driving force behind this immunosuppression, through suppression of proinflammatory gene production and subsequent immune cell activation, proliferation and effector function. A better understanding of epigenetics and post-septic immunosuppression can improve our diagnostic tools and may be an important potential source of novel molecular targets for new therapies. This review will discuss important pathways of immune cell activation affected by severe sepsis, and highlight pathways of epigenetic regulation that may be involved in post-septic immunosuppression. |
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Authors:
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William F Carson; Karen A Cavassani; Yali Dou; Steven L Kunkel |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-03-01 |
Journal Detail:
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Title: Epigenetics : official journal of the DNA Methylation Society Volume: 6 ISSN: 1559-2308 ISO Abbreviation: Epigenetics Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-03-23 Completed Date: 2011-07-22 Revised Date: 2011-10-28 |
Medline Journal Info:
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Nlm Unique ID: 101265293 Medline TA: Epigenetics Country: United States |
Other Details:
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Languages: eng Pagination: 273-83 Citation Subset: IM |
Affiliation:
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Department of Pathology, University of Michigan, Ann Arbor, USA. wfcarson@umich.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Proliferation Epigenesis, Genetic* Humans Immune Tolerance / genetics* Immunity, Innate / genetics Models, Biological Sepsis / genetics*, immunology* |
| Grant Support | |
ID/Acronym/Agency:
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HL089216/HL/NHLBI NIH HHS; HL31237/HL/NHLBI NIH HHS; R01 HL031237-27/HL/NHLBI NIH HHS |
| Comments/Corrections | |
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