Jeffrey C. Rathmell
Studies how nutrients and metabolic pathways control lymphocyte growth, differentiation and function; his lab helped show that effector and regulatory CD4 T cells rely on different fuel programmes, glycolysis versus lipid oxidation (in mouse cells).
Chair, Ben May Department for Cancer Research, Virginia and D. K. Ludwig Chair Professor and Director, Ludwig Center for Metastasis Research, University of Chicago (since 2025) · Cornelius Vanderbilt Professor of Immunobiology and Director, Vanderbilt Center for Immunobiology, Vanderbilt University Medical Center (2015–2025) · faculty, Duke University (2003–2015) · postdoc with Craig B. Thompson, University of Chicago and University of Pennsylvania · PhD in immunology, Stanford University
Rathmell Lab, Ben May Department for Cancer Research, University of Chicago (Chicago, Illinois, USA) ↗ Lab lineagetrained under Craig B. Thompson →
Jeffrey Rathmell was senior author of the 2011 Journal of Immunology study (MIC2011) comparing the metabolism of mouse CD4 T cells grown as effector (Th1, Th2, Th17) or induced regulatory cells. Effector cells carried a lot of the glucose transporter Glut1 and were strongly glycolytic, while regulatory cells oxidised more lipid and had more active AMPK. Blocking lipid oxidation with etomoxir suppressed regulatory T-cell generation and also prevented the rise in regulatory cells caused by rapamycin, which links the pro-regulatory effect of mTOR inhibition to lipid oxidation. mTOR activity itself was not measured; the mTOR step rests on the drug effects.
Rathmell earned his PhD in immunology at Stanford University and did postdoctoral work with Craig B. Thompson at the University of Chicago and the University of Pennsylvania. He started his own lab at Duke University in 2003, moved to Vanderbilt in 2015 to direct the Vanderbilt Center for Immunobiology, and in July 2025 became chair of the Ben May Department for Cancer Research at the University of Chicago. His lab works on how nutrient environments, for example in obesity or inflamed tissue, shape immune-cell metabolism and cancer immunotherapy.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets MIC2011 Senior author: effector CD4 T cells are glycolytic while regulatory T cells depend on lipid oxidation, which also underlies the rapamycin-driven increase in regulatory cells (mouse cells). |
Co-authors in the Atlas
People with a profile here who share at least one study with Jeffrey C. Rathmell.
- Ryan D. Michalek T-cell metabolism researcher who, as a postdoc with Jeffrey Rathmell, showed that effector CD4 T cells rely on glycolysis while regulatory T cells rely on lipid oxidation, which ties the pro-Treg effect of rapamycin to fatty acid oxidation; he later moved into metabolomics in industry
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