EJHaem · 2026
Rare But Specific B-Cell Receptor Reactivity Against Coxsackievirus A24 in Primary Central Nervous System Lymphomas.
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Kos Igor Age, Cetin Onur, Fadle Natalie, Regitz Evi, Preuss Klaus-Dieter, Lohse Stefan, Smola Sigrun, Hartmann Sylvia, Fend Falko, Klingel Karin, Scherer Florian, Schorb Elisabeth, Bewarder Moritz, Staber Philipp, Thurner Lorenz
Аннотация
INTRODUCTION: Primary central nervous system lymphoma (PCNSL) remains a distinct and aggressive malignancy whose underlying antigenic triggers are largely unknown. While autoantigens such as neurabin-I and SAMD14 have been implicated, the potential role of infectious agents in driving clonal B-cell receptor selection within the central nervous system remains less understood.
METHODS: A viral proteome microarray screening approach encompassing 158 viral entities was utilized to test tumor-derived recombinant B-cell receptors from PCNSL. Furthermore, we analyzed a validation cohort comprising 22 PCNSL patients and tested expanded control sera from 188 healthy individuals. Functional assays were performed to confirm B-cell receptor activation and downstream signaling upon cognate antigen engagement.
RESULTS: Screening identified a distinct B-cell receptor reactivity directed against Coxsackievirus A24 in a PCNSL case, which was completely absent across non-PCNSL lymphomas. Validation testing in an independent cohort confirmed rare reactivity (1/22, 4.55%). Control serum analysis revealed weak reactivity in 1 out of 188 healthy individuals (0.53%). Functional assays demonstrated that the Coxsackievirus A24-derived antigen is capable of triggering antigen-specific receptor signaling.
CONCLUSION: We report the first evidence linking PCNSL B-cell receptor reactivity to a viral antigen, identifying Coxsackievirus A24 as a rare ligand. While functional assays confirm the capacity for receptor activation, the findings must be interpreted cautiously as hypothesis-generating. Further investigation in larger independent cohorts is required to determine whether viral antigens play any meaningful pathogenic role in this malignancy.
TRIAL REGISTRATION: The authors have confirmed clinical trial registration is not needed for this submission.
METHODS: A viral proteome microarray screening approach encompassing 158 viral entities was utilized to test tumor-derived recombinant B-cell receptors from PCNSL. Furthermore, we analyzed a validation cohort comprising 22 PCNSL patients and tested expanded control sera from 188 healthy individuals. Functional assays were performed to confirm B-cell receptor activation and downstream signaling upon cognate antigen engagement.
RESULTS: Screening identified a distinct B-cell receptor reactivity directed against Coxsackievirus A24 in a PCNSL case, which was completely absent across non-PCNSL lymphomas. Validation testing in an independent cohort confirmed rare reactivity (1/22, 4.55%). Control serum analysis revealed weak reactivity in 1 out of 188 healthy individuals (0.53%). Functional assays demonstrated that the Coxsackievirus A24-derived antigen is capable of triggering antigen-specific receptor signaling.
CONCLUSION: We report the first evidence linking PCNSL B-cell receptor reactivity to a viral antigen, identifying Coxsackievirus A24 as a rare ligand. While functional assays confirm the capacity for receptor activation, the findings must be interpreted cautiously as hypothesis-generating. Further investigation in larger independent cohorts is required to determine whether viral antigens play any meaningful pathogenic role in this malignancy.
TRIAL REGISTRATION: The authors have confirmed clinical trial registration is not needed for this submission.