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Epigenetic Epidemiology of Inflammation and Rheumatoid Arthritis

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Epigenetic Epidemiology
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Abstract

The field of epigenetic research has evolved dramatically in recent years and has given valuable insight into regulation and dysregulation of gene expression in health and disease. The knowledge of the mechanisms controlling epigenetic changes increased, and in more and more diseases, a role for epigenetics could be found. Rheumatoid arthritis is a chronic inflammatory, autoimmune disease that leads to joint destruction but also affects other tissues and organs. Its etiology is not yet clarified, but a combination of the genetic background and environmental factors is proposed to trigger the onset of the disease. Epigenetic changes might be the link between non-genetic risk factors and development of symptoms. Changes in DNA methylation and histone modifications have been detected in patients with RA and have been found to promote inflammation and joint destruction. Future studies will have to show which epigenetic changes are causative factors and which are induced at a later stage by the chronic inflammatory environment seen in the disease. This knowledge holds the potential for new preventive, predictive, and therapeutic opportunities in RA.

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Abbreviations

ACPA:

anti-citrullinated peptide autoantibodies

DNMT:

DNA methyltransferase

EBV:

Epstein Barr virus

H3:

histone 3

H4:

histone 4

HAT:

histone acetylases

HDACs:

histone deacetylases

HERV:

human endogenous retrovirus

IGF:

Insulin-like growth factor

IL:

interleukin

MHC:

major histocompatibility complex

PBMCs:

peripheral blood mononuclear cells

RA:

rheumatoid arthritis

SFN:

Sulforaphane

SLE:

systemic lupus erythematodes

TLRs:

Toll-like receptors

Xi:

inactivated X chromosome

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Correspondence to Caroline Ospelt .

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Ospelt, C., Gay, S. (2022). Epigenetic Epidemiology of Inflammation and Rheumatoid Arthritis. In: Michels, K.B. (eds) Epigenetic Epidemiology. Springer, Cham. https://doi.org/10.1007/978-3-030-94475-9_15

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