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Your search keyword '"Chen, Zongming E."' showing total 2 results
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2 results on '"Chen, Zongming E."'

1. Ikaros Inhibits Group 3 Innate Lymphoid Cell Development and Function by Suppressing the Aryl Hydrocarbon Receptor Pathway.

Author

Li, Shiyang, Heller, Jennifer J., Bostick, John W., Lee, Aileen, Schjerven, Hilde, Kastner, Philippe, Chan, Susan, Chen, Zongming E., and Zhou, Liang

Subjects
*INNATE lymphoid cells, *ARYL hydrocarbon receptors, *TRANSCRIPTION factors, *ZINC-finger proteins, *IMMUNE response
Abstract

Summary Group 3 innate lymphoid cells (ILC3s) expressing the transcription factor (TF) RORγt are important for the defense and homeostasis of host intestinal tissues. The zinc finger TF Ikaros, encoded by Ikzf1 , is essential for the development of RORγt + fetal lymphoid tissue inducer (LTi) cells and lymphoid organogenesis, but its role in postnatal ILC3s is unknown. Here, we show that small-intestinal ILC3s had lower Ikaros expression than ILC precursors and other ILC subsets. Ikaros inhibited ILC3s in a cell-intrinsic manner through zinc-finger-dependent inhibition of transcriptional activity of the aryl hydrocarbon receptor, a key regulator of ILC3 maintenance and function. Ablation of Ikzf1 in RORγt + ILC3s resulted in increased expansion and cytokine production of intestinal ILC3s and protection against infection and colitis. Therefore, in contrast to being required for LTi development, Ikaros inhibits postnatal ILC3 development and function to regulate gut immune responses at steady state and in disease. [ABSTRACT FROM AUTHOR]

Published
2016
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2. Requirement of Mitochondrial Transcription Factor A in Tissue-Resident Regulatory T Cell Maintenance and Function.

Author

Fu Z, Ye J, Dean JW, Bostick JW, Weinberg SE, Xiong L, Oliff KN, Chen ZE, Avram D, Chandel NS, and Zhou L

Subjects
Animals, Cell Proliferation genetics, Chromatin metabolism, Colitis genetics, Colitis metabolism, DNA Methylation, DNA-Binding Proteins genetics, Female, Forkhead Transcription Factors genetics, Glycolysis, Inflammation genetics, Inflammation metabolism, Melanoma, Experimental genetics, Melanoma, Experimental metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondrial Proteins genetics, Oxidative Phosphorylation, RNA-Seq, T-Lymphocytes, Regulatory immunology, Transcription Factors genetics, Transcriptome genetics, Transplantation, Homologous, DNA-Binding Proteins metabolism, Forkhead Transcription Factors metabolism, Melanoma, Experimental immunology, Mitochondria metabolism, Mitochondrial Proteins metabolism, T-Lymphocytes, Regulatory metabolism, Transcription Factors metabolism
Abstract

Regulatory T cells (Tregs) are pivotal for immune suppression. Cellular metabolism is important for Treg homeostasis and function. However, the exact role of mitochondrial respiration in Tregs remains elusive. Mitochondrial transcription factor A (Tfam) is essential for mitochondrial respiration and controls mitochondrial DNA replication, transcription, and packaging. Here, we show that genetic ablation of Tfam in Tregs impairs Treg maintenance in non-lymphoid tissues in the steady state and in tumors. Tfam-deficient Tregs have reduced proliferation and Foxp3 expression upon glucose deprivation in vitro. Tfam deficiency preferentially affects gene activation in Tregs through regulation of DNA methylation, with enhanced methylation in the TSDR of the Foxp3 locus. Deletion of Tfam in Tregs affects Treg homing and stability, resulting in tissue inflammation in colitis, but enhances tumor rejection. Thus, our work reveals a critical role of Tfam-mediated mitochondrial respiration in Tregs to regulate inflammation and anti-tumor immunity., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2019
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