Research Overview

Dr. Zhou is interested in deciphering molecular and cellular mechanisms that regulate tissue homeostasis and inflammation, and to understand how dys-regulation of these processes leads to inflammatory disorders. To achieve this goal, the Zhou lab applies interdisciplinary approaches across immunology, systems biology, molecular and cellular biology, with a research focus on the communication between immune and non-immune cell types and between cells and their microenvironment. 

Research Background

Xu Zhou is a Principal Investigator in the Division of Gastroenterology, Hepatology and Nutrition, at the department of Pediatrics of Boston Children’s Hospital. He is a member of faculty at Harvard Medical School. Dr. Zhou earned a B.S. from Peking University studying viral capsule protein of Hepatitis virus B. He obtained a Ph.D. with Dr. Erin O’Shea in the Department of Molecular and Cellular Biology at Harvard University, studying systems biology and transcriptional regulation. He then completed his postdoctoral training with Dr. Ruslan Medzhitov in the Department of Immunobiology at Yale University School of Medicine, investigating the mechanisms of tissue homeostasis and inflammation. The Zhou lab opened at Boston Children’s Hospital in 2021.

Publications

  1. Regulation of inflammatory responses by pH-dependent transcriptional condensates. Cell. 2025 Oct 02; 188(20):5632-5652.e25. View Abstract
  2. Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections. Immunity. 2025 Sep 09; 58(9):2190-2207.e13. View Abstract
  3. Divergence in a eukaryotic transcription factor's co-TF dependence involves multiple intrinsically disordered regions. Nat Commun. 2025 Jun 18; 16(1):5340. View Abstract
  4. How can concepts from ecology enable insights about cellular communities? Cell Syst. 2024 Oct 16; 15(10):885-890. View Abstract
  5. Reshaping the tumor microenvironment by degrading glycoimmune checkpoints Siglec-7 and -9. bioRxiv. 2024 Oct 12. View Abstract
  6. Control of Inflammatory Response by Tissue Microenvironment. bioRxiv. 2024 May 14. View Abstract
  7. pH sensing at the intersection of tissue homeostasis and inflammation. Trends Immunol. 2023 10; 44(10):807-825. View Abstract
  8. Hematopoietic anomalies fuels multiple sclerosis. Life Med. 2022 Oct; 1(2):52-54. View Abstract
  9. Tissue Homeostasis and Inflammation. Annu Rev Immunol. 2021 04 26; 39:557-581. View Abstract
  10. Principles of Cell Circuits for Tissue Repair and Fibrosis. iScience. 2020 Feb 21; 23(2):100841. View Abstract
  11. Desynchronization of the molecular clock contributes to the heterogeneity of the inflammatory response. Sci Signal. 2019 03 05; 12(571). View Abstract
  12. Siglec-15 as an immune suppressor and potential target for normalization cancer immunotherapy. Nat Med. 2019 04; 25(4):656-666. View Abstract
  13. Adipocyte OGT governs diet-induced hyperphagia and obesity. Nat Commun. 2018 11 30; 9(1):5103. View Abstract
  14. Endocytosis as a stabilizing mechanism for tissue homeostasis. Proc Natl Acad Sci U S A. 2018 02 20; 115(8):E1926-E1935. View Abstract
  15. Circuit Design Features of a Stable Two-Cell System. Cell. 2018 02 08; 172(4):744-757.e17. View Abstract
  16. Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus. Nat Med. 2017 Aug; 23(8):997-1003. View Abstract
  17. Evolution of reduced co-activator dependence led to target expansion of a starvation response pathway. Elife. 2017 05 09; 6. View Abstract
  18. A computational approach to map nucleosome positions and alternative chromatin states with base pair resolution. Elife. 2016 09 13; 5. View Abstract
  19. Two-signal requirement for growth-promoting function of Yap in hepatocytes. Elife. 2015 Feb 10; 4. View Abstract
  20. Integrated approaches reveal determinants of genome-wide binding and function of the transcription factor Pho4. Mol Cell. 2011 Jun 24; 42(6):826-36. View Abstract
  21. Identification of the critical regions in hepatitis B virus preS required for its stability. J Pept Sci. 2008 Mar; 14(3):307-12. View Abstract
  22. Serum levels of preS antigen (HBpreSAg) in chronic hepatitis B virus infected patients. Virol J. 2007 Sep 24; 4:93. View Abstract

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