The impact of age-related hypomethylated DNA on immune signaling upon cellular demise

Lauren A Urban; Annie Trinh; Eric Pearlman; Albert Siryaporn; Timothy L Downing

doi:10.1016/j.it.2021.04.005

The impact of age-related hypomethylated DNA on immune signaling upon cellular demise

Trends Immunol. 2021 Jun;42(6):464-468. doi: 10.1016/j.it.2021.04.005. Epub 2021 May 11.

Authors

Lauren A Urban¹, Annie Trinh¹, Eric Pearlman², Albert Siryaporn³, Timothy L Downing⁴

Affiliations

¹ Department of Microbiology and Molecular Genetics, University of California-Irvine, Irvine, CA 92697, USA; The Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California-Irvine, Irvine, CA 92697, USA.
² Institute for Immunology, University of California-Irvine, Irvine, CA 92697, USA; Department of Ophthalmology, University of California-Irvine, Irvine, CA 92697, USA; Department of Physiology and Biophysics, University of California-Irvine, Irvine, CA 92697, USA.
³ Department of Physics and Astronomy, University of California-Irvine, Irvine, CA 92697, USA; Department of Molecular Biology and Biochemistry, University of California-Irvine, Irvine, CA 92697, USA.
⁴ Department of Microbiology and Molecular Genetics, University of California-Irvine, Irvine, CA 92697, USA; The Edwards Lifesciences Center for Advanced Cardiovascular Technology, University of California-Irvine, Irvine, CA 92697, USA; Department of Biomedical Engineering, University of California-Irvine, Irvine, CA 92697, USA. Electronic address: tim.downing@uci.edutim.downing@uci.edu.

Abstract

Aging is associated with decreased antigen-specific immunity and increased chronic inflammation. While DNA-sensing pathways might be involved, the molecular factors underlying these age-related aberrancies in immune signaling are unclear. Here, we consider the potential role of aging-induced hypomethylated DNA as a putative stimulant of age-associated inflammation.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

MeSH terms

Aging*
DNA
Humans
Inflammation
Signal Transduction*

Substances

DNA

Abstract

Publication types

MeSH terms

Substances

Grants and funding