Journal
AUTOIMMUNITY
Volume 41, Issue 4, Pages 329-335Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08916930802024889
Keywords
immune senescence; epigenetic mechanisms; DNA methylation; autoimmunity
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Funding
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES017885] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG020628, R01AG028268, R56AG020628, P30AG013283, P30AG024824] Funding Source: NIH RePORTER
- NIAMS NIH HHS [R01 AR042525] Funding Source: Medline
- NIA NIH HHS [P30 AG013283, R56 AG020628, R01 AG028268, R01AG020628, R01 AG020628, AG024824, R01AG028268, P30 AG024824] Funding Source: Medline
- NIEHS NIH HHS [P30 ES017885] Funding Source: Medline
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Immune senescence is associated with a decline in T- and B-cell immune responses. It is, therefore, perhaps surprising that aging is linked to the appearance of serological and clinical autoimmunity. Here we review the mechanisms that contribute to the increase in inflammatory and autoimmune responses in aging. The bulk of this review will focus on aging-associated changes in epigenetic mechanisms, and in particular DNA methylation, as this has emerged as an attractive mechanistic link between aging and autoimmunity.
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