Julia Qu

Associate Professor of Immunology and Immune Therapeutics

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Overview

The research in the Qu lab focuses on lung immunity, inflammation, and diseases, spanning acute injury, chronic conditions, infectious diseases, and lung cancer—the leading cause of cancer-related mortality worldwide. Using mouse and human co-clinical models and state-of-the-art technologies, the Qu group is trying to elucidate the cellular and molecular mechanisms underlying lung homeostasis and diseases development, progression, and therapy resistance, for preventive, prognostic, and therapeutic purposes, and is developing innovative therapies for lung cancer, the most devastating cancer type.

As the primary organ for gas exchange, the lung constantly encounters challenges from the external environment. The lung immune system, particularly the innate immunity, plays a crucial role in guarding the lung against these threats and maintaining lung homeostasis. The Qu research team is investigating the mechanisms underlying pulmonary immune regulation and its deregulation, particularly the innate immune components, in promoting lung inflammation and disease development and progression. At the cellular level, they mainly focus on lung epithelial cells and macrophages, the key sentinels in the lung and the main culprits of lung diseases. At the molecular level, they mainly focus on NF-κB and STAT signaling pathways, master regulators of cell survival, proliferation, and immunity.

Research Funding

  • The NF-kappaB modulator PDLIM2 as an intrinsic checkpoint of alveolar macrophages critical for lung innate immunity, inflammation and diseases
    NIH · R01HL177140 · Apr 1, 2025 – Jan 31, 2029 · Role: Principal Investigator
  • Mechanistic difference of NF-kappaB in lung physiology and tumorigenesis
    NIH · R01CA258614 · Aug 24, 2022 – Jul 31, 2027 · Role: Principal Investigator
  • Structural and molecular dissection of NF-kappaB regulation by the ubiquitin E3 ligase PDLIM2 in lung innate immunity and diseases
    NIH · R01GM144890 · Mar 10, 2022 – Feb 28, 2026 · Role: Principal Investigator
  • Clinicopathological significance of PDLIM2 in HIV/AIDS-related malignancies caused by KSHV
    NIH · R21CA189703 · Jul 1, 2015 – Jun 30, 2018 · Role: Principal Investigator

Publications

  • Alveolar Macrophages Inherently Express Programmed Death-1 Ligand 1 for Optimal Protective Immunity and Tolerance. J Immunol. 2021 07 01; 207(1):110-114.. View in PubMed
  • PDLIM2 repression by ROS in alveolar macrophages promotes lung tumorigenesis. JCI Insight. 2021 03 08; 6(5).. View in PubMed
  • Methods to Detect NF-κB Activity in Tumor-Associated Macrophage (TAM) Populations. Methods Mol Biol. 2021; 2366:213-241.. View in PubMed
  • Dual but not single PD-1 or TIM-3 blockade enhances oncolytic virotherapy in refractory lung cancer. J Immunother Cancer. 2020 05; 8(1).. View in PubMed
  • Causative role of PDLIM2 epigenetic repression in lung cancer and therapeutic resistance. Nat Commun. 2019 11 22; 10(1):5324.. View in PubMed
  • NF-κB RelA renders tumor-associated macrophages resistant to and capable of directly suppressing CD8+ T cells for tumor promotion. Oncoimmunology. 2018; 7(6):e1435250.. View in PubMed
  • Murine Bronchoalveolar Lavage. Bio Protoc. 2017 May 20; 7(10).. View in PubMed
  • Isolation of Murine Alveolar Type II Epithelial Cells. Bio Protoc. 2017 May 20; 7(10).. View in PubMed
  • Myeloid STAT3 Promotes Lung Tumorigenesis by Transforming Tumor Immunosurveillance into Tumor-Promoting Inflammation. Cancer Immunol Res. 2017 03; 5(3):257-268.. View in PubMed
  • Kaposi’s sarcoma herpesvirus (KSHV) microRNA K12-1 functions as an oncogene by activating NF-κB/IL-6/STAT3 signaling. Oncotarget. 2016 May 31; 7(22):33363-73.. View in PubMed