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Abstract
Chimeric antigen receptor T cell (CAR-T) therapy has transformed the treatment of hematologic malignancies, yet, severe inflammatory toxicities continue to limit its broader use. In this issue of the JCI, Goala et al. uncovered a mechanistic link between IFN-γ–driven inflammation and disrupted neutrophil homeostasis, revealing that cytokine release syndrome (CRS) and immune cell–associated hematologic toxicity (ICAHT) stem from a shared biological pathway. Using IL-2Ra–deficient mice and patient samples, they showed that IFN-γ suppressed IL-17A and granulocyte colony-stimulating factor (G-CSF), disrupting granulopoiesis and neutrophil survival. Strikingly, IFN-γ blockade eased both CRS and neutropenia without diminishing CAR-T efficacy, suggesting a path toward safer, better-tolerated cell therapies.
Authors
Stefanie R. Bailey, Marcela V. Maus
Usage data is cumulative from January 2026 through March 2026.
| Usage | JCI | PMC |
|---|---|---|
| Text version | 2,423 | 323 |
| 559 | 58 | |
| Figure | 278 | 0 |
| Supplemental data | 111 | 4 |
| Citation downloads | 70 | 0 |
| Totals | 3,441 | 385 |
| Total Views | 3,826 | |
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Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)