Qian Zhang
Xuetao Cao
1 Laboratory of Immunity and Inflammation, College of Life Sciences, Nankai University, Tianjin 300071, China;
2 National Key Laboratory of Medical Immunology, Institute of Immunology, Navy Military Medical University, Shanghai 200433, China;
3 Department of Immunology, Center for Immunotherapy, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China
Funds: We thank Dr. Bingjing Wang for helpful discussion. This work was supported by grants from the National Natural Science Foundation of China (81788101, 81922032) and CAMS Innovation Fund for Medical Sciences (2016-12M-1-003).
Received Date: 2020-07-07
Rev Recd Date:2020-09-15
Publish Date:2021-03-12
Abstract
Abstract
TET2, a member of ten-eleven translocation (TET) family as α-ketoglutarate- and Fe2+-dependent dioxygenase catalyzing the iterative oxidation of 5-methylcytosine (5mC), has been widely recognized to be an important regulator for normal hematopoiesis especially myelopoiesis. Mutation and dysregulation of TET2 contribute to the development of multiple hematological malignancies. Recent studies reveal that TET2 also plays an important role in innate immune homeostasis by promoting DNA demethylation or independent of its enzymatic activity. Here, we focus on the functions of TET2 in the initiation and resolution of inflammation through epigenetic regulation and signaling network. In addition, we highlight regulation of TET2 at various molecular levels as well as the correlated inflammatory diseases, which will provide the insight to intervene in the pathological process caused by TET2 dysregulation.Keywords: TET2,
innate immune response,
DNA demethylation,
inflammatory resolution,
inflammatory diseases
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