The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy

Abstract Background Immune effector cell-associated neurotoxicity syndrome (ICANS) is a common and potentially life-threatening complication of chimeric antigen receptor (CAR) T cell therapy. The underlying mechanisms of ICANS remain incompletely understood and are unlikely to be explained by cytoki...

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Main Authors: I-Na Lu, Louisa Müller-Miny, Carolin Krekeler, Phyllis Fung-Yi Cheung, Georgia Antonopoulou, Astrid Jeibmann, Andreas Schulte-Mecklenbeck, Kornelius Kerl, Simon Call, Christian Reicherts, Annalen Bleckmann, Matthias Stelljes, Georg Lenz, Heinz Wiendl, Gerd Meyer zu Hörste, Oliver M. Grauer
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Genome Medicine
Online Access:https://doi.org/10.1186/s13073-025-01498-6
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author I-Na Lu
Louisa Müller-Miny
Carolin Krekeler
Phyllis Fung-Yi Cheung
Georgia Antonopoulou
Astrid Jeibmann
Andreas Schulte-Mecklenbeck
Kornelius Kerl
Simon Call
Christian Reicherts
Annalen Bleckmann
Matthias Stelljes
Georg Lenz
Heinz Wiendl
Gerd Meyer zu Hörste
Oliver M. Grauer
author_facet I-Na Lu
Louisa Müller-Miny
Carolin Krekeler
Phyllis Fung-Yi Cheung
Georgia Antonopoulou
Astrid Jeibmann
Andreas Schulte-Mecklenbeck
Kornelius Kerl
Simon Call
Christian Reicherts
Annalen Bleckmann
Matthias Stelljes
Georg Lenz
Heinz Wiendl
Gerd Meyer zu Hörste
Oliver M. Grauer
author_sort I-Na Lu
collection DOAJ
description Abstract Background Immune effector cell-associated neurotoxicity syndrome (ICANS) is a common and potentially life-threatening complication of chimeric antigen receptor (CAR) T cell therapy. The underlying mechanisms of ICANS remain incompletely understood and are unlikely to be explained by cytokine excess alone. Methods We analyzed paired peripheral blood and cerebrospinal fluid (CSF) samples from CAR T cell–treated patients who developed ICANS (n = 11) within 5–21 days post-infusion. ICANS severity was graded as follows: grade 1 (n = 3), grade 2 (n = 4), grade 3 (n = 1), and grade 4 (n = 3). Control samples were obtained from patients with idiopathic intracranial hypertension, functional neurological disorders, and multiple sclerosis. We employed single-cell RNA sequencing (scRNA-seq) and flow cytometry to profile immune cell populations and performed multi-modal spatial transcriptomics and immunofluorescence on postmortem choroid plexus and brain tissue from a patient with fatal grade 4 ICANS. Results We identified a distinct population of proliferating, cytotoxic T cells characterized by CXCR6 expression, enriched in CD4 + CAR T cells and predominantly localized in ICANS CSF. These CXCR6 + T cells were largely absent from control CSF samples. Spatial mapping of postmortem brain tissue revealed widespread infiltration of myeloid cells and a striking spatial association between CXCR6 + T cells and CXCL16-expressing myeloid cells in both the choroid plexus and brain parenchyma. Notably, CSF levels of CXCL16 positively correlated with ICANS severity across the cohort, from grade 1 to grade 4. Conclusions Our findings implicate the CXCL16/CXCR6 axis in the recruitment of cytotoxic CAR CD4 + T cells to the central nervous system (CNS) during ICANS. This interaction may be linked to neuroinflammatory processes and severity stratification in ICANS pathogenesis. These results provide a mechanistic rationale for exploring CXCL16/CXCR6 as a potential biomarker and therapeutic target in CAR T cell-associated neurotoxicity.
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spelling doaj-art-a9dc471607f24ffcbe922b745b599b202025-08-20T04:02:56ZengBMCGenome Medicine1756-994X2025-06-0117111410.1186/s13073-025-01498-6The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapyI-Na Lu0Louisa Müller-Miny1Carolin Krekeler2Phyllis Fung-Yi Cheung3Georgia Antonopoulou4Astrid Jeibmann5Andreas Schulte-Mecklenbeck6Kornelius Kerl7Simon Call8Christian Reicherts9Annalen Bleckmann10Matthias Stelljes11Georg Lenz12Heinz Wiendl13Gerd Meyer zu Hörste14Oliver M. Grauer15Department of Neurology With Institute of Translational Neurology, University Hospital MünsterDepartment of Neurology With Institute of Translational Neurology, University Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterSpatiotemporal Tumor Heterogeneity, German Cancer Consortium (DKTK), partner site Essen, a partnership between German Cancer Research Center (DKFZ) and University Hospital EssenBridge Institute of Experimental Tumor Therapy, West German Cancer Center, University Hospital Essen, University of Duisburg-EssenInstitute of Neuropathology, University Hospital MünsterDepartment of Neurology With Institute of Translational Neurology, University Hospital MünsterDepartment of Pediatric Hematology and Oncology, University Children’s Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital MünsterDepartment of Neurology With Institute of Translational Neurology, University Hospital MünsterDepartment of Neurology With Institute of Translational Neurology, University Hospital MünsterDepartment of Neurology With Institute of Translational Neurology, University Hospital MünsterAbstract Background Immune effector cell-associated neurotoxicity syndrome (ICANS) is a common and potentially life-threatening complication of chimeric antigen receptor (CAR) T cell therapy. The underlying mechanisms of ICANS remain incompletely understood and are unlikely to be explained by cytokine excess alone. Methods We analyzed paired peripheral blood and cerebrospinal fluid (CSF) samples from CAR T cell–treated patients who developed ICANS (n = 11) within 5–21 days post-infusion. ICANS severity was graded as follows: grade 1 (n = 3), grade 2 (n = 4), grade 3 (n = 1), and grade 4 (n = 3). Control samples were obtained from patients with idiopathic intracranial hypertension, functional neurological disorders, and multiple sclerosis. We employed single-cell RNA sequencing (scRNA-seq) and flow cytometry to profile immune cell populations and performed multi-modal spatial transcriptomics and immunofluorescence on postmortem choroid plexus and brain tissue from a patient with fatal grade 4 ICANS. Results We identified a distinct population of proliferating, cytotoxic T cells characterized by CXCR6 expression, enriched in CD4 + CAR T cells and predominantly localized in ICANS CSF. These CXCR6 + T cells were largely absent from control CSF samples. Spatial mapping of postmortem brain tissue revealed widespread infiltration of myeloid cells and a striking spatial association between CXCR6 + T cells and CXCL16-expressing myeloid cells in both the choroid plexus and brain parenchyma. Notably, CSF levels of CXCL16 positively correlated with ICANS severity across the cohort, from grade 1 to grade 4. Conclusions Our findings implicate the CXCL16/CXCR6 axis in the recruitment of cytotoxic CAR CD4 + T cells to the central nervous system (CNS) during ICANS. This interaction may be linked to neuroinflammatory processes and severity stratification in ICANS pathogenesis. These results provide a mechanistic rationale for exploring CXCL16/CXCR6 as a potential biomarker and therapeutic target in CAR T cell-associated neurotoxicity.https://doi.org/10.1186/s13073-025-01498-6
spellingShingle I-Na Lu
Louisa Müller-Miny
Carolin Krekeler
Phyllis Fung-Yi Cheung
Georgia Antonopoulou
Astrid Jeibmann
Andreas Schulte-Mecklenbeck
Kornelius Kerl
Simon Call
Christian Reicherts
Annalen Bleckmann
Matthias Stelljes
Georg Lenz
Heinz Wiendl
Gerd Meyer zu Hörste
Oliver M. Grauer
The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
Genome Medicine
title The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
title_full The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
title_fullStr The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
title_full_unstemmed The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
title_short The CXCL16/CXCR6 axis is linked to immune effector cell-associated neurotoxicity in chimeric antigen receptor (CAR) T cell therapy
title_sort cxcl16 cxcr6 axis is linked to immune effector cell associated neurotoxicity in chimeric antigen receptor car t cell therapy
url https://doi.org/10.1186/s13073-025-01498-6
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