Hong Pan

Chinese Academy of Sciences

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Lintao Cai

Shenzhen Institutes of Advanced Technology

Lanlan Liu

Shenzhen Third People’s Hospital

Yifan Ma

Zhejiang Wanli University

Mingbin Zheng

Shenzhen Third People’s Hospital

Ting Yin

Wuyi University

Ai-Qing Ma

Shenzhen Institutes of Advanced Technology

Huamei He

Shenzhen Institutes of Advanced Technology

Ruijing Liang

Shenzhen Institutes of Advanced Technology

Ce Wang

Beijing University of Technology

Ze Chen

City University of Hong Kong

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Chinese Academy of Sciences

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Shenzhen Institutes of Advanced Technology

University of Chinese Academy of Sciences

Sun Yat-sen University

Shanghai Jiao Tong University

Guangdong Medical College

Huazhong University of Science and Technology

Peking University

Southern Medical University

Zhejiang University

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Bio‐Orthogonal T Cell Targeting Strategy for Robustly Enhancing Cytotoxicity against Tumor Cells

Small (2018)

Wenjun Li Hong Pan Huamei He Xiaoqing Meng Qian Ren

Abstract T cells can kill tumor cells by cell surface immunological recognition, but low affinity for tumor‐associated antigens could lead to T cell off‐target effects. Herein, a universal T cell targeting strategy based on bio‐orthogonal chemistry and glycol‐metabolic engineering is introduced to enhance recognition and cytotoxicity of T cells in tumor immunotherapy. Three kinds of bicycle [6.1.0] nonyne (BCN)‐modified sugars are designed and synthesized, in which Ac 4 ManN‐BCN shows efficient incorporation into wide tumor cells with a BCN motif on surface glycans. Meanwhile, activated T cells are treated with Ac 4 GalNAz to introduce azide (N 3 ) on the cell surface, initiating specific tumor targeting through a bio‐orthogonal click reaction between N 3 and BCN. This artificial targeting strategy remarkably enhances recognition and migration of T cells to tumor cells, and increases the cytotoxicity 2 to 4 times for T cells against different kinds of tumor cells. Surprisingly, based on this strategy, the T cells even exhibit similar cytotoxicity with the chimeric antigen receptor T‐cell against Raji cells in vitro at the effector: target cell ratios (E:T) of 1:1. Such a universal bio‐orthogonal T cell‐targeting strategy might further broaden applications of T cell therapy against tumors and provide a new strategy for T cell modification.

Raji cell

Cancer Immunotherapy

10.1002/smll.201804383

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Citations (49)

Smart gold nanocages for mild heat-triggered drug release and breaking chemoresistance

Journal of Controlled Release (2020)

Huamei He Lanlan Liu Shengping Zhang Mingbin Zheng Ai-Qing Ma

Nanocages

10.1016/j.jconrel.2020.04.029

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Citations (48)

Retinal-conjugated pH-sensitive micelles induce tumor senescence for boosting breast cancer chemotherapy

Biomaterials (2016)

Yijuan Zhang Ping Li Hong Pan Lanlan Liu Manyi Ji

Senescence

10.1016/j.biomaterials.2016.01.023

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Citations (46)

IR-780 dye loaded chemiluminescent organic nanoparticles with near-infrared emission for hydrogen peroxide detection and imaging

Nanomedicine Nanotechnology Biology and Medicine (2018)

Tao Jiang Yayun Wu Hong Pan Guanjun Deng Pengfei Zhang

10.1016/j.nano.2017.11.027

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Nanoengineered CAR‐T Biohybrids for Solid Tumor Immunotherapy with Microenvironment Photothermal‐Remodeling Strategy

Small (2021)

Ze Chen Hong Pan Yingmei Luo Ting Yin Baozhen Zhang

Abstract Chimeric antigen receptor T cell (CAR‐T) therapy has shown remarkable clinical success in eradicating hematologic malignancies. However, hostile microenvironment in solid tumors severely prevents CAR‐T cells migrating, infiltrating, and killing. Herein, a nanoengineered CAR‐T strategy is reported for enhancing solid tumor therapy through bioorthogonal conjugation with a nano‐photosensitizer (indocyanine green nanoparticles, INPs) as a microenvironment modulator. INPs engineered CAR‐T biohybrids (CT‐INPs) not only retain the original activities and functions of CAR‐T cells, but it is further armed with fluorescent tracing and microenvironment remodeling abilities. Irradiated with laser, CT‐INPs demonstrate that mild photothermal intervention destroys the extracellular matrix, expanded blood vessels, loosened compact tissue, and stimulated chemokine secretion without damping CAR‐T cell activities. Those regulations induce an immune‐favorable tumor microenvironment for recruitment and infiltration of CT‐INPs. CT‐INPs triggered photothermal effects collapse the physical and immunological barriers of solid tumor, and robustly boosted CAR‐T immunotherapy. Therefore, CAR‐T biohybrids provide reliable treatment strategy for solid tumor immunotherapy via microenvironment reconstruction.

10.1002/smll.202007494

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Citations (72)

Lymphatic-targeted cationic liposomes: A robust vaccine adjuvant for promoting long-term immunological memory

Vaccine (2014)

Ce Wang Peng Liu Yan Zhuang Ping Li Bo-Ling Jiang

Priming (agriculture)

10.1016/j.vaccine.2014.07.081

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Citations (80)

Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-κB and p38 MAPK signaling pathways

AJP Lung Cellular and Molecular Physiology (2013)

Hong Pan Yijuan Zhang Zichao Luo Ping Li Lanlan Liu

Since avian influenza virus H5N1-induced hypercytokemia plays a key role in acute lung injury, understanding its molecular mechanism is highly desirable for discovering therapeutic targets against H5N1 infection. In the present study, we investigated the role of autophagy in H5N1-induced lung inflammation by using H5N1 pseudotyped viral particles (H5N1pps). The results showed that H5N1pps significantly induced autophagy both in A549 human lung epithelial cells and in mouse lung tissues, which was primarily due to hemagglutinin (HA) of H5N1 virus. Blocking autophagy with 3-methyladenine (an autophagy inhibitor) or siRNA knockdown of autophagy-related genes (beclin1 and atg5) dramatically attenuated H5N1pp-induced proinflammatory cytokines and chemokines, such as IL-1β, TNF-α, IL-6, CCL2, and CCL5, both in vitro and in vivo. Autophagy-mediated inflammatory responses involved the activation of NF-κB and p38 MAPK signaling pathways, which required the presence of clathrin but did not rely on p62 or autophagosome-lysosome fusion. On the other hand, the activation of NF-κB also promoted H5N1pp-induced autophagosome formation. These data indicated a positive feedback loop between autophagy and NF-κB signaling cascade, which could exacerbate H5N1pp-induced lung inflammation. Our data demonstrated an essential role of autophagy in H5N1pp-triggered inflammatory responses, and targeting the autophagic pathway could be a promising strategy to treat H5N1 virus-caused lung inflammation.

Proinflammatory cytokine

Sequestosome 1

Autophagosome

BECN1

10.1152/ajplung.00147.2013

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Citations (73)

Nanovaccine loaded with poly I:C and STAT3 siRNA robustly elicits anti-tumor immune responses through modulating tumor-associated dendritic cells in vivo

Biomaterials (2014)

Zichao Luo Ce Wang Huqiang Yi Ping Li Hong Pan

TLR3

CD86