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Yinggui Yang on Muck Rack

Yinggui Yang

As seen in: Nature
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Articles

GITR activation potentiates anti-tumor immunity of tumor-infiltrating lymphocytes expanded from glioblastoma by rescuing exhaustion - Oncogene

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By Jiayi Zhou, Yinggui Yang, Ran Ye, Jiani Lin, Huiyi Feng, Xiaojuan Pei, Mingzhen Li, Xinzhi Yang, Penghui Zhou, Jie Mao, Zhuohao Liu, Dinglan Wu, Jiangfan Peng
| Nature Verified
Abstract Autologous tumor-infiltrating lymphocyte (TIL) therapy holds transformative potential for solid tumors, yet its efficacy in glioblastoma remains limited by T cell exhaustion and immunosuppression. In the current study, we optimized an effective and reliable method for in vitro expansion of TILs from glioblastoma lesions and assessed their tumor-killing capacity both in vitro and in vivo.
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Exogenous Epstein–Barr virus nuclear antigen 1 induces ADAR1-driven tumor resistance against immunotherapy - Signal Transduction and Targeted Therapy

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By Changlin Liu, Zhiqiang Sun, Yanqing Zhou, Xuefeng Gao, Yuping Zhong, Xiaomin Luo, Chenci Wang, Yuanbin Zhang, Chuping Ni, Manli Peng, Weiquan Jian, Yinggui Yang, Xuewen Zhang, Yichang Ren, Xinqi Gong, Min Zhao, Xia Guo, Jianjun Chen, Xin Li Verified
| Nature Verified
Abstract Immune checkpoint blockade (ICB) therapy continues to face limitations due to tumor resistance linked to suppressed interferon (IFN) signaling. This suppression can be attributed to multiple mechanisms, among which viral pathogens represent a compelling though not yet fully elucidated factor. Here, we demonstrate that exogenous Epstein–Barr virus-encoded EBNA1 drives immunosuppression via enhanced RNA-editing enzyme ADAR1-mediated RNA editing.
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Interferon-induced transmembrane protein-1 competitively blocks Ephrin receptor A2-mediated Epstein–Barr virus entry into epithelial cells - Nature Microbiology

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By Xiaomin Luo, Ting Gong, Xinqi Gong, Qingyou Zheng, Yinggui Yang, Dinglan Wu
| Nature Verified
Abstract Epstein–Barr virus (EBV) can infect both B cells and epithelial cells (ECs), causing diseases such as mononucleosis and cancer. It enters ECs via Ephrin receptor A2 (EphA2). The function of interferon-induced transmembrane protein-1 (IFITM1) in EBV infection of ECs remains elusive.
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