Contribution of Dysregulated DNA Methylation to Autoimmunity

被引:10
|
作者
Funes, Samanta C. [1 ]
Fernandez-Fierro, Ayleen [2 ]
Rebolledo-Zelada, Diego [2 ]
Mackern-Oberti, Juan P. [3 ]
Kalergis, Alexis M. [2 ,4 ]
机构
[1] Univ Nacl San Luis UNSL, Consejo Nacl Invest Cient & Tecn CONICET, Inst Multidisciplinario Invest Biol San Luis IMIB, RA-5700 San Luis, Argentina
[2] Pontificia Univ Catolica Chile, Millennium Inst Immunol & Immunotherapy, Dept Genet Mol & Microbiol, Fac Ciencias Biol, Santiago 8320000, Chile
[3] Univ Nacl Cuyo, Fac Ciencias Med, Inst Med & Biol Expt Cuyo IMBECU CONICET, RA-5500 Mendoza, Argentina
[4] Pontificia Univ Catolica Chile, Fac Med, Dept Endocrinol, Santiago 8320000, Chile
关键词
DNA methylation; epigenetic; systemic autoimmunity; rheumatoid arthritis; CpG; NAIVE CD4+T CELLS; LUPUS-LIKE DISEASE; RHEUMATOID-ARTHRITIS; T-CELLS; PROMOTER METHYLATION; GENE-EXPRESSION; GENOME; PATTERNS; HYPOMETHYLATION; DEMETHYLATION;
D O I
10.3390/ijms222111892
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epigenetic mechanisms, such as DNA methylation, histone modifications, and non-coding RNAs are known regulators of gene expression and genomic stability in cell growth, development, and differentiation. Because epigenetic mechanisms can regulate several immune system elements, epigenetic alterations have been found in several autoimmune diseases. The purpose of this review is to discuss the epigenetic modifications, mainly DNA methylation, involved in autoimmune diseases in which T cells play a significant role. For example, Rheumatoid Arthritis and Systemic Lupus Erythematosus display differential gene methylation, mostly hypomethylated 5 '-C-phosphate-G-3 ' (CpG) sites that may associate with disease activity. However, a clear association between DNA methylation, gene expression, and disease pathogenesis must be demonstrated. A better understanding of the impact of epigenetic modifications on the onset of autoimmunity will contribute to the design of novel therapeutic approaches for these diseases.
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页数:19
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