
Harvey Cantor
· ProfessorHarvard University · Strategy
Active 1956–2025
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About
Harvey Cantor is a Professor of Immunology at Harvard Medical School, based at the Dana Farber Cancer Institute. His lab studies the development and function of T-cell subsets, focusing on how different T-cell lineages recognize MHC class I and II molecules and mediate distinct immunological functions. Early research indicated that the thymus gives rise to two major T-cell lineages, and his work has contributed to understanding cell-mediated immunity, natural killer cells, and regulatory and effector lineages within the CD8+ T-cell subset. Current research in his lab includes defining regulatory T cell lineages that inhibit autoimmune disease and regulate anti-viral and anti-tumor immunity. His team has studied the role of the Helios transcription factor in maintaining Treg stability and self-tolerance. Additionally, his research involves studying non-classical CD8+ T-cells recognizing viral peptides presented by MHC-E molecules to understand their role in anti-viral and anti-tumor immunity, especially in the context of immune evasion by tumors. His work also explores genetic and epigenetic factors controlling the tumor microenvironment and investigates the immune system's contribution to Alzheimer's Disease. His research aims to enhance understanding of cellular and molecular mechanisms to improve vaccine design and immunotherapy.
Research topics
- Genetics
- Biology
- Immunology
- Cancer research
- Internal medicine
- Medicine
Selected publications
Overcoming Immune Checkpoint Blockade Resistance via EZH2 Inhibition
Trends in Immunology · 2020 · 86 citations
Mechanism of EBV inducing anti-tumour immunity and its therapeutic use
Nature · 2020 · 85 citations
Proceedings of the National Academy of Sciences · 2022-02-17 · 64 citations
articleOpen accessSenior authorCorrespondingSignificance CD11c + microglia enriched for osteopontin (OPN) expression appear at distinct stages of brain development, aging, and several neurodegenerative disorders. Whether coexpression of CD11c and OPN results from microglial activation or represents a part of a subset-specific genetic program is unknown. We find that this CD11c + microglial subset is formed before birth upon uptake of apoptotic neurons. Our analysis also suggests that it represents a stable subset that requires OPN to medi…
Cell Reports · 2019-11-01 · 60 citations
articleOpen accessCorrespondingcheckpoint that enforces suppressive activity and acts as a gatekeeper of GC entry.
Proceedings of the National Academy of Sciences · 2023-02-02 · 55 citations
articleOpen accessSenior authorAlzheimer’s disease (AD) is the most common form of incurable dementia and represents a critical public health issue as the world’s population ages. Although microglial dysregulation is a cardinal feature of AD, the extensive heterogeneity of these immunological cells in the brain has impeded our understanding of their contribution to this disease. Here, we identify a pathogenic microglial subset which expresses the CD11c surface marker as the sole producer of Osteopontin (OPN) in the 5XFAD mous…
Recent grants
NIH · $778k · 1999
NIH · $3.4M · 1997
NIH · $3.2M · 2015
Frequent coauthors
- 189 shared
F W Shen
Liaocheng University
- 138 shared
L McVay-Boudreau
- 132 shared
J Hugenberger
United States Public Health Service
- 123 shared
Diane D. Eardley
- 118 shared
John D. Kemp
- 87 shared
Richard K. Gershon
- 67 shared
Linrong Lu
Renji Hospital
- 66 shared
Hye‐Jung Kim
Wonkwang University
Education
- 1980
Ph.D., Immunology
Harvard University
- 1976
M.D.
Harvard Medical School
- 1972
B.A., Biology
University of California, Berkeley
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