Epigenetic regulation of inflammation by CxxC domain-containing proteins
- PMID: 34935162
- DOI: 10.1111/imr.13056
Epigenetic regulation of inflammation by CxxC domain-containing proteins
Abstract
Epigenetic regulation of gene transcription in the immune system is important for proper control of protective and pathogenic inflammation. Aberrant epigenetic modifications are often associated with dysregulation of the immune cells, including lymphocytes and macrophages, leading to pathogenic inflammation and autoimmune diseases. Two classical epigenetic markers-histone modifications and DNA cytosine methylation, the latter is the 5 position of the cytosine base in the context of CpG dinucleotides-play multiple roles in the immune system. CxxC domain-containing proteins, which basically bind to the non-methylated CpG (i.e., epigenetic "readers"), often function as "writers" of the epigenetic markers via their catalytic domain within the proteins or by interacting with other epigenetic modifiers. We herein report the most recent advances in our understanding of the functions of CxxC domain-containing proteins in the immune system and inflammation, mainly focusing on T cells and macrophages.
Keywords: DNA methylation; helper T cells; ten-eleven translocation (TET) proteins; trithorax.
© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
References
REFERENCES
-
- Nakayama T, Hirahara K, Onodera A, et al. Th2 cells in health and disease. Annu Rev Immunol. 2017;35:53-84.
-
- Liu K, Min J. Structural basis for the recognition of non-methylated DNA by the CXXC domain. J Mol Biol. 2020;432(6):1674-1686.
-
- Deaton AM, Bird A. CpG islands and the regulation of transcription. Genes Dev. 2011;25(10):1010-1022.
-
- Blackledge NP, Zhou JC, Tolstorukov MY, Farcas AM, Park PJ, Klose RJ. CpG islands recruit a histone H3 lysine 36 demethylase. Mol Cell. 2010;38(2):179-190.
-
- Xiong X, Tu S, Wang J, Luo S, Yan X. CXXC5: a novel regulator and coordinator of TGF-beta, BMP and Wnt signaling. J Cell Mol Med. 2019;23(2):740-749.
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