Lieping Chen
陈列平
MD, PhD
United Technologies Corporation Professor of Cancer Immunology; Co-Director, Cancer Immunology Program, Yale Cancer Center联合技术公司癌症免疫学教授;耶鲁癌症中心癌症免疫学项目联合主任
👥Biography 个人简介
Lieping Chen, MD, PhD is the United Technologies Corporation Professor of Cancer Immunology and Co-Director of the Cancer Immunology Program at Yale Cancer Center, Yale School of Medicine. He is widely recognized as the discoverer of PD-L1 (which he originally termed B7-H1), the principal ligand for the PD-1 immune checkpoint. Working at the Mayo Clinic in 1999, Dr. Chen identified B7-H1 (now called PD-L1 or CD274) as a novel B7 family member that delivers co-inhibitory signals to T cells, and subsequently demonstrated in a landmark 2002 paper that B7-H1/PD-L1 is overexpressed on human cancer cells and suppresses tumor-specific T cell responses — directly explaining a major mechanism of cancer immune escape. This work provided a crucial molecular link between the PD-1 receptor and tumor immune evasion, and was instrumental in motivating the clinical development of anti-PD-L1 antibodies including atezolizumab, durvalumab, and avelumab. Dr. Chen's laboratory has also characterized multiple other B7 family members and their roles in immune regulation, and has been a leading voice in defining rational combination immunotherapy strategies. He is frequently cited among the most impactful scientists in the checkpoint immunotherapy revolution and has been involved in intellectual property proceedings regarding PD-L1 discovery priority. He has published more than 300 papers and has received numerous honors for his foundational contributions to cancer immunology.
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
PD-L1 (B7-H1) Discovery and Characterization as Tumor Immune Escape Molecule
Discovered and cloned B7-H1 (PD-L1/CD274) in 1999, characterizing it as a novel co-inhibitory B7 family ligand; subsequently demonstrated in 2002 that B7-H1 is broadly overexpressed on human tumor cells — including carcinomas of the lung, ovary, colon, and melanoma — where it suppresses tumor-reactive T cells, establishing the molecular mechanism of PD-1 pathway-mediated cancer immune escape and the rationale for anti-PD-L1 therapy.
B7 Family Co-inhibitory Ligand Biology
Has systematically characterized the B7 family of co-stimulatory and co-inhibitory ligands and their receptors, including B7-H3, B7-H4, HHLA2, and others, defining their expression patterns in tumors, immune regulatory functions, and potential as therapeutic targets — expanding the conceptual framework for co-inhibitory pathway-targeted cancer immunotherapy beyond PD-1/PD-L1.
Translational Research Connecting PD-L1 Expression to Clinical Outcomes
Conducted pioneering translational studies demonstrating that PD-L1 expression in tumor tissue correlates with poor prognosis and immune evasion across multiple cancer types, providing the scientific basis for PD-L1 immunohistochemistry as a companion diagnostic biomarker for checkpoint inhibitor therapy — a cornerstone of precision immuno-oncology patient selection.
Rational Combination Immunotherapy Strategies
Has been an intellectual leader in defining how PD-1/PD-L1 blockade can be combined with vaccines, adoptive cell transfer, and other checkpoint inhibitors, and has advocated for multi-target IO approaches based on mechanistic understanding of how tumors co-opt multiple co-inhibitory pathways simultaneously to resist single-agent checkpoint blockade.
Representative Works 代表性著作
B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion
Nature Medicine (1999)
Discovery paper identifying and cloning B7-H1 (PD-L1) as a novel co-inhibitory B7 family ligand, founding the PD-L1 field.
Involvement of B7-H1 in the induction of tumor-specific T-cell suppression and tolerance
Journal of Experimental Medicine (2002)
Landmark paper demonstrating B7-H1/PD-L1 overexpression on human tumor cells mediates tumor-specific T cell suppression, establishing the molecular mechanism of cancer immune escape via the PD-1 pathway.
The B7-H3 ligand gene is associated with programmed death-1
Proceedings of the National Academy of Sciences (2004)
Characterized B7-H3 as an additional B7 family co-inhibitory molecule with roles in T cell regulation and tumor immune evasion.
Coexpression of Tim-3 and PD-1 identifies a CD8+ T-cell exhaustion phenotype in mouse models of glioma
Nature Medicine (2012)
Demonstrated co-expression of multiple co-inhibitory receptors (Tim-3, PD-1) defines deeply exhausted tumor-infiltrating T cells, informing combination checkpoint immunotherapy strategies.
🏆Awards & Recognition 奖项与荣誉
📄Data Sources 数据来源
Last updated: 2026-04-06 | All information from publicly available academic sources
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