Kristen N. Pollizzi
Immunologist trained in Jonathan Powell's lab at Johns Hopkins who used gene deletions in mice to show how the two mTOR complexes push killer T cells toward effector or memory fates
Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine (Powell lab, 2011–2016; latest PubMed affiliation)
Portrait: LinkedIn (same photo as JCI author interview)
CD8 T cells are the immune system's killer cells. After an infection, most become short-lived effectors that attack, and a few become long-lived memory cells that guard against the next infection. Kristen Pollizzi's 2015 study in the Journal of Clinical Investigation, with Jonathan Powell as senior author, used mice whose T cells lacked Tsc2, Rheb or Rictor to separate the roles of the two mTOR complexes. With Tsc2 gone, mTORC1 stayed switched on: the cells burned glucose hard, made more of the killing molecules IFN-gamma, TNF and granzyme B, and controlled tumours better, but they ended up terminally differentiated, fewer in number after a month, and formed no memory. With Rheb gone, mTORC1 was off while mTORC2 still worked: these cells failed as effectors and kept memory-like features, yet they did not respond when the mice met the same antigen again, which the authors traced to defects in their metabolism.
The message is that mTOR activity tunes the balance between attack and memory, and that a T cell needs the right amount of each complex at the right time. That matters for vaccine design and for cancer treatments that rely on T cells. Pollizzi was also a co-author on the 2011 Nature Immunology paper from the same lab showing that mTORC1 and mTORC2 steer helper (CD4) T cells into different lineages.
PubMed lists 11 papers for Pollizzi between 2011 and 2016, all with the Powell group at the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins. They include a 2015 PLoS One study showing that cell size after activation can be used to track mTOR activity and predict whether a T cell becomes an effector or a long-lived cell, and reviews on mTOR and T cell metabolism in Nature Reviews Immunology (2014) and Trends in Immunology (2015). No later publications or current position could be found.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2011 | A | The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2 DEL2011 Co-author on the study showing that mTORC1 and mTORC2 selectively program distinct CD4 helper T-cell lineages. |
| 2015 | A | mTORC1 and mTORC2 selectively regulate CD8+ T cell differentiation POL2015 First author: used Tsc2, Rheb and Rictor deletion in T cells to show that constant mTORC1 drives glycolytic, terminally differentiated effectors with no memory, while loss of mTORC1 gives memory-like cells that still fail on rechallenge. |
Co-authors in the Atlas 4
People with a profile here who share at least one study with Kristen N. Pollizzi.
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- Adam T. Waickman 2 shared studies Immunologist who trained in Jonathan Powell's mTOR and T cell lab at Johns Hopkins and now studies human immune responses to dengue virus at SUNY Upstate Medical University
- Greg M. Delgoffe 2 shared studies Showed as a graduate student in Jonathan Powell's lab that T cells lacking mTOR become regulatory rather than effector T cells, and that mTORC1 and mTORC2 steer different helper-T-cell fates
- Jonathan D. Powell 2 shared studies Showed that T cells lacking mTOR become regulatory T cells instead of effector cells, and that mTORC1 and mTORC2 each steer a different type of helper T cell
- Maureen R. Horton Pulmonary physician-scientist who studies immune mechanisms of lung inflammation and fibrosis
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