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Cytokines in CAR T Cell-Associated Neurotoxicity.
Juliane Gust1,2, Rafael Ponce3, W Conrad Liles4
1Department of Neurology, University of Washington, Seattle, WA, United States.
Frontiers in Immunology
|January 4, 2021
Summary
Chimeric antigen receptor (CAR) T cell therapy can cause neurotoxicity, known as immune effector cell-associated neurotoxicity syndrome (ICANS). This review explores cytokine roles in ICANS and potential therapeutic strategies.
Area of Science:
- Immunology
- Neuroscience
- Oncology
Background:
- Chimeric antigen receptor (CAR) T cell therapy offers new hope for hematologic malignancies.
- Neurotoxicity, termed immune effector cell-associated neurotoxicity syndrome (ICANS), is a significant complication.
- ICANS presents with diverse neurological symptoms, from delirium to seizures and cerebral edema.
Purpose of the Study:
- To review the role of cytokines in CAR T-cell-induced neurotoxicity (ICANS).
- To explore potential preventive and therapeutic strategies for ICANS.
- To contextualize ICANS within other inflammatory neurological conditions.
Main Methods:
- Systematic review of studies correlating inflammatory mediators with ICANS risk.
- Detailed examination of cytokine (IL-1, IL-6, IL-15, GM-CSF) pathophysiologic impacts on the CNS.
- Comparison of ICANS mechanisms with other systemic inflammatory encephalopathies.
Main Results:
- Cytokine release is implicated in ICANS pathogenesis.
- Specific cytokines like IL-1, IL-6, IL-15, and GM-CSF are key candidates.
- Understanding neurovascular unit and glial cell responses to inflammation is crucial.
Conclusions:
- Cytokine-driven inflammation is central to ICANS.
- Targeting cytokines like IL-1 and IL-6 shows therapeutic promise.
- Further research is needed to elucidate ICANS mechanisms and develop effective treatments.
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