Epigenetic Epidemiology pp 289-305 | Cite as
Epigenetic Epidemiology of Inflammation and Rheumatoid Arthritis
Abstract
The field of epigenetic research has evolved dramatically in recent years and has given valuable insight in 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 which 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.
Keywords
Rheumatoid Arthritis Rheumatoid Arthritis Patient Transposable Element Histone Modification Epigenetic ChangeAbbreviations
- ACPA
anti-citrullinated peptide auto-antibodies
- 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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