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Immune senescence, epigenetics and autoimmunity
dc.contributor.authorRay, D
dc.contributor.authorYung, R
dc.coverage.spatialUnited States
dc.date.accessioned2024-05-06T18:56:45Z
dc.date.available2024-05-06T18:56:45Z
dc.date.issued2018-11-01
dc.identifier.issn1521-6616
dc.identifier.issn1521-7035
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pubmed/29654845
dc.identifier.urihttps://hdl.handle.net/2027.42/193079en
dc.description.abstractAging of the immune system in humans and animals is characterized by a decline in both adaptive and innate immune responses. Paradoxically, aging is also associated with a state of chronic inflammation (“inflammaging”) and an increased likelihood of developing autoimmune diseases. Epigenetic changes in non-dividing and dividing cells, including immune cells, due to environmental factors contribute to the inflammation and autoimmunity that characterize both the state and diseases of aging. Here, we review the epigenetic mechanisms involved in the development of immune senescence and autoimmunity in old age.
dc.format.mediumPrint-Electronic
dc.languageeng
dc.publisherElsevier
dc.subjectAutoimmunity
dc.subjectEpigenetics
dc.subjectImmune senescence
dc.subjectInflammation
dc.subjectAdaptive Immunity
dc.subjectAging
dc.subjectAutoimmune Diseases
dc.subjectAutoimmunity
dc.subjectEpigenesis, Genetic
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectImmunosenescence
dc.subjectInflammation
dc.titleImmune senescence, epigenetics and autoimmunity
dc.typeArticle
dc.identifier.pmid29654845
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/193079/2/nihms-1024318.pdf
dc.identifier.doi10.1016/j.clim.2018.04.002
dc.identifier.doihttps://dx.doi.org/10.7302/22724
dc.identifier.sourceClinical Immunology
dc.description.versionPublished version
dc.date.updated2024-05-06T18:56:45Z
dc.identifier.orcid0000-0002-8181-027X
dc.identifier.volume196
dc.identifier.startpage59
dc.identifier.endpage63
dc.identifier.name-orcidRay, D
dc.identifier.name-orcidYung, R; 0000-0002-8181-027X
dc.working.doi10.7302/22724en
dc.owningcollnameInternal Medicine, Department of


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