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Abstract
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.
Acknowledgements
This work was supported in part by the National Institute of Health grants RO1AG020628 and RO1AG028268 (RY), Veteran Affairs Merit Review grant (RY), and the University of Michigan Claude Pepper Older Americans Independence Center (AG024824) (AG).
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.