Journal
AUTOIMMUNITY
Volume 41, Issue 4, Pages 278-286Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08916930802024616
Keywords
epigenetics; DNA methylation; lupus; psoriasis; atopic dermatitis; vitiligo
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Funding
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR042525] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES015214] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG025877] Funding Source: NIH RePORTER
- NIAMS NIH HHS [AR42525, R01 AR042525, R01 AR042525-08] Funding Source: Medline
- NIA NIH HHS [AG25877, R01 AG025877-04, R01 AG025877] Funding Source: Medline
- NIEHS NIH HHS [R01 ES015214-04, R01 ES015214, ES015214] Funding Source: Medline
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Epigenetic mechanisms are essential for normal development and function of the immune system. Similarly, a failure to maintain epigenetic homeostasis in the immune response due to factors including environmental influences, leads to aberrant gene expression, contributing to immune dysfunction and in some cases the development of autoimmunity in genetically predisposed individuals. This is exemplified by systemic lupus erythematosus, where environmentally induced epigenetic changes contribute to disease pathogenesis in those genetically predisposed. Similar interactions between genetically determined susceptibility and environmental factors are implicated in other systemic autoimmune diseases such as rheumatoid arthritis and scleroderma, as well as in organ specific autoimmunity. The skin is exposed to a wide variety of environmental agents, including UV radiation, and is prone to the development of autoimmune conditions such as atopic dermatitis, psoriasis and some forms of vitiligo, depending on environmental and genetic influences. Herein we review how disruption of epigenetic mechanisms can alter immune function using lupus as an example, and summarize how similar mechanisms may contribute to other human autoimmune rheumatic and skin diseases.
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