About

Xiang Zhou is Professor of Sociology at Harvard University. He is also a faculty affiliate at the Weatherhead Center for International Affairs, Harvard Institute for Quantitative Social Science, Harvard Center for Population and Development Studies, and Fairbank Center for Chinese Studies. His research broadly concerns inequality, education, causal inference, quantitative methods, and contemporary China. Zhou's scholarly work has been published in leading peer-reviewed journals including the American Sociological Review, American Journal of Sociology, Social Forces, Journal of Political Economy, American Journal of Political Science, Journal of the Royal Statistical Society Series B, and Proceedings of the National Academy of Sciences (PNAS). Prior to joining Harvard, he worked as a postdoctoral research associate at Princeton University. He earned his PhD in Sociology and Statistics from the University of Michigan in 2015.

Research topics

• Biology
• Immunology
• Computer Science
• Artificial Intelligence
• Cell biology
• Mathematical optimization
• Mathematics
• Cancer research
• Internal medicine
• Medicine
• Neuroscience

Selected publications

• FTO controls CD8+ T cell survival and effector response by modulating m6A methylation of Fas

  Cell Death and Disease · 2025-04-15 · 4 citations

  articleOpen access

  Abstract Functional CD8 + T cell immunity is essential for immune surveillance and host defense against infection and tumors. Epigenetic mechanisms, particularly RNA modification, in controlling CD8 + T cell immune response is not fully elucidated. Here, by T cell-specific deletion of fat mass and obesity-associated protein (FTO), a critical N6-methyladenosine (m 6 A) demethylase, we revealed that FTO was indispensable for adequate CD8 + T cell immune response and protective function. FTO ablation led to considerable cell death in activated CD8 + T cells, which was attributed to cell apoptosis. MeRIP-seq analysis revealed an increase in m 6 A methylation on Fas mRNA in FTO-deficient CD8 + T cells. The loss of FTO promoted Fas expression via enhancing the Fas mRNA stability, which depended on the m 6 A reader insulin-like growth factor-2 mRNA-biding proteins 3 (IGF2BP3). Mutation of the Fas m 6 A sites or knockdown IGF2BP3 could normalize the upregulated Fas expression and apoptosis levels caused by FTO ablation in CD8 + T cells. Our findings delineate a novel epigenetic regulatory mechanism of FTO-mediated m 6 A modification in supporting CD8 + T cell survival and effector responses, providing new insights into understanding the post-transcriptional regulation in CD8 + T cell immunological functions and the potential therapeutic intervention.

  PublisherDOI

• Crop leaf disease detection with additive gated convolution and hierarchical attention fusion

  Scientific Reports · 2025-11-25 · 1 citations

  articleOpen access

  Crop leaf disease detection plays a crucial role in ensuring healthy crop growth and improving food security. Disease features are often small and have blurry edges, while background interference is strong, making precise detection a significant challenge. Although YOLO-based methods perform well in object detection, they still struggle to effectively handle the extraction of lesion details and background noise interference when applied to crop leaf disease detection. To address these challenges, this study introduces an innovative crop leaf disease detection approach built upon the YOLO, named AG-HAF. This method proposed two modules, the additive gated convolutional unit (AGCU), which introduces a gating mechanism to dynamically adjust the importance of features, enhancing the detection of small and blurry lesions, improving nonlinear feature modeling, and suppressing irrelevant background interference. Hierarchical Attention Fusion Module (HACFM), which utilizes a hierarchical attention mechanism to optimize the fusion of multi-scale features, enhancing the representation and semantic information of disease regions, and further improving the model's adaptability to complex backgrounds. Ablation and comparative experiments show that AG-HAF outperforms existing methods across various metrics, particularly excelling in disease detecting in complex backgrounds and small lesions, demonstrating significant potential for practical applications.

  PublisherOA PDFDOI

• Large-area flexible thermal control films via balancing low solar absorptivity and low infrared emissivity

  Applied Surface Science · 2025-12-05

  article
  PublisherDOI

• HHIP protein interactions in lung cells provide insight into COPD pathogenesis

  Human Molecular Genetics · 2025-02-10 · 3 citations

  articleOpen access

  Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. The primary causes of COPD are environmental, including cigarette smoking; however, genetic susceptibility also contributes to COPD risk. Genome-Wide Association Studies (GWASes) have revealed more than 80 genetic loci associated with COPD, leading to the identification of multiple COPD GWAS genes. However, the biological relationships between the identified COPD susceptibility genes are largely unknown. Genes associated with a complex disease are often in close network proximity, i.e. their protein products often interact directly with each other and/or similar proteins. In this study, we use affinity purification mass spectrometry (AP-MS) to identify protein interactions with HHIP, a well-established COPD GWAS gene which is part of the sonic hedgehog pathway, in two disease-relevant lung cell lines (IMR90 and 16HBE). To better understand the network neighborhood of HHIP, its proximity to the protein products of other COPD GWAS genes, and its functional role in COPD pathogenesis, we create HUBRIS, a protein-protein interaction network compiled from 8 publicly available databases. We identified both common and cell type-specific protein-protein interactors of HHIP. We find that our newly identified interactions shorten the network distance between HHIP and the protein products of several COPD GWAS genes, including DSP, MFAP2, TET2, and FBLN5. These new shorter paths include proteins that are encoded by genes involved in extracellular matrix and tissue organization. We found and validated interactions to proteins that provide new insights into COPD pathobiology, including CAVIN1 (IMR90) and TP53 (16HBE). The newly discovered HHIP interactions with CAVIN1 and TP53 implicate HHIP in response to oxidative stress.

  PublisherOA PDFDOI

• Non-mutated human tau stimulates Alzheimer’s disease-relevant neurodegeneration in a microglia-dependent manner

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-11

  preprintOpen access

  Abstract The accumulation of abnormal, non-mutated tau protein is a key pathological hallmark of Alzheimer’s disease (AD). Despite its strong association with disease progression, the mechanisms by which tau drives neurodegeneration in the brain remain poorly understood. Here, we selectively expressed non-mutated or mutated human microtubule-associated protein tau ( hMAPT ) in neurons across the brain and observed neurodegeneration in the hippocampus, especially associated with non-mutated human tau. Single-nuclei RNA sequencing confirmed a selective loss of hippocampal excitatory neurons by the wild-type tau and revealed the upregulation of neurodegeneration-related pathways in the affected populations. The accumulation of phosphorylated tau was accompanied by cellular stress in neurons and reactive gliosis in multiple brain regions. Notably, the lifelong absence of microglia significantly and differentially influenced the extent of neurodegeneration in the hippocampus and thalamus. Therefore, our study established an AD-relevant tauopathy mouse model, elucidated both neuron-intrinsic and neuron-extrinsic responses, and highlighted critical and complex roles of microglia in modulating tau-driven neurodegeneration.

  PublisherDOI

• Non-mutated human tau stimulates Alzheimer’s disease-relevant neurodegeneration in a microglia-dependent manner

  Scientific Reports · 2025-07-29 · 1 citations

  articleOpen access

  The accumulation of abnormal, non-mutated tau protein is a key pathological hallmark of Alzheimer's disease (AD). Despite its strong association with disease progression, the mechanisms by which tau drives neurodegeneration in the brain remain poorly understood. Here, we selectively expressed non-mutated or mutated human microtubule-associated protein tau (hMAPT) in neurons across the mouse brain and observed neurodegeneration in the hippocampus, especially associated with non-mutated human tau. Single-nuclei RNA sequencing confirmed a selective loss of hippocampal excitatory neurons by the wild-type tau and revealed the upregulation of neurodegeneration-related pathways in the affected populations. The accumulation of phosphorylated tau was accompanied by cellular stress in neurons and reactive gliosis in multiple brain regions. Notably, the lifelong absence of microglia significantly and differentially influenced the extent of neurodegeneration in the hippocampus and thalamus. Therefore, our study established an AD-relevant tauopathy mouse model, elucidated both neuron-intrinsic and neuron-extrinsic responses, and highlighted critical and complex roles of microglia in modulating tau-driven neurodegeneration.

  PublisherOA PDFDOI

• Large Area Flexible Thermal Control Films via Excellent Low Solar Absorptivity and Low Infrared Emissivity

  SSRN Electronic Journal · 2025-01-01

  preprintOpen access
  PublisherDOI

• Research on UAV Attitude Adjustment Strategy for Forest Fire Monitoring

  Lecture notes in networks and systems · 2025-01-01

  book-chapter
  PublisherDOI

• Airway Epithelium Derived from Induced Pluripotent Stem Cells to Model Asthma Susceptibility Loci

  American Journal of Respiratory and Critical Care Medicine · 2025-07-28 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• Zinc finger protein Zfp335 is required for T cell homeostatic proliferation through regulating Lmnb1

  Cell & Bioscience · 2025-10-14 · 2 citations

  articleOpen access

  T cell homeostasis is crucial for maintaining T cell population size and upcoming protective immunity in the peripheral organs. However, it remains largely unknown about the intracellular molecules and pathways beyond IL-7R signaling. Zfp335, as a key transcription factor, is involved in the multiple-stage development of thymocytes, and effector and memory T cell differentiation during immune responses. In current study, we found an upregulated expression of ZFP335 in both CD4+ and CD8+ T cells during peripheral homeostasis. In an adoptive transfer model, Zfp335−/− T cells failed to undergo homeostatic proliferation without survival defect. Consistently, deletion of Zfp335 impaired T cell proliferation in in vitro culture with IL-7. Furthermore, both RNA-Sequencing and qPCR analysis showed that Zfp335 significantly affected the expression of cell cycle-related genes. Mechanistically, Zfp335 directly binds to the promoter of Lmnb1 gene and regulates its transcription. Overexpression of Lmnb1 significantly rescued the impaired proliferation of Zfp335−/− T cells. Our results reveal a previously unrecognized role of Zfp335 in maintaining T cell homeostasis within peripheral lymphoid tissues. Specifically, Zfp335 promotes the homeostatic proliferation of naïve T cells by directly modulating the expression of the Lmnb1 gene which ensuring the capacity of immune system.

  PublisherOA PDFDOI

Recent grants

• Systems Modeling Guided Bone regeneration

  NIH · $243k · 2016–2017

• NIH Grant U01HL11156001

  NIH · $389k · 2013

• NIH Grant R01LM01018503

  NIH · $314k · 2013

• NIH Grant R01LM010185

  NIH · $635k · 2015

• Systems Modeling Guided Bone regeneration

  NIH · $3.2M · 2016–2023

Frequent coauthors

• Edwin K. Silverman

  Harvard University

  164 shared

• Stephen T.C. Wong

  Cornell University

  112 shared

• Daniel Bernstein

  Stanford University

  81 shared

• David A. Schwartz

  University of Colorado Denver

  75 shared

• Benjamin A. Raby

  Harvard University

  75 shared

• Michael H. Cho

  Brigham and Women's Hospital

  74 shared

• Ivan P. Moskowitz

  University of Chicago

  72 shared

• Xiaozhong Luo

  National Institutes of Health

  72 shared

Education

• Ph.D., Cell Biology

  Chinese Academy of Medical Sciences & Peking Union Medical College

• Pharm D., Pharmacology

  West China University of Medical Sciences