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ORIGINAL RESEARCH article

Front. Immunol.

Sec. B Cell Biology

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1528471

CD19 + B Cell Depletion: A Novel Strategy to Alleviating Ischemic Stroke Damage

Provisionally accepted
Yu Xu Yu Xu 1Jing Peng Jing Peng 2Yizhong Yan Yizhong Yan 2Min Gao Min Gao 3Hongjing Zang Hongjing Zang 3Lamei Cheng Lamei Cheng 1,2YU ZHOU YU ZHOU 4*
  • 1 Central South University, Changsha, Hunan Province, China
  • 2 National Engineering Research Center of Human Stem Cells, Changsha, Hunan Province, China
  • 3 Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China
  • 4 Department of Neurosurgery, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China

The final, formatted version of the article will be published soon.

    Ischemic stroke, accounting for approximately 80% of all stroke cases, is a major public health challenge and a leading cause of death and disability worldwide. Current treatments primarily involve thrombolytic therapy, limited to a 4.5-hour window due to the risk of complications, underscoring the need for new therapeutic targets. Systemic inflammation plays a critical role in stroke progression, with immune cells infiltrating the brain and exacerbating damage. B cells, in particular, have been implicated in stroke pathogenesis, although their exact role remains contentious. This study examines anti-CD19 antibody (aCD19 Ab) treatment in a stroke model to determine if CD19 + B cell depletion can reduce infarct size and alleviate inflammation. Results This study investigated whether temporary inhibition of B-cell activity using an aCD19 Ab could alleviate ischemic brain injury in a stroke mouse model by regulating cerebral and systemic immune reactions. Mice subjected to middle cerebral artery occlusion (MCAO) exhibited significant reductions in infarct size and brain edema, prolonged post-MCAO survival, and improved behavioral outcomes following aCD19 Ab treatment. Transmission electron microscopy (TEM) and Computed Tomography Angiography (CTA) results revealed a reduction in microvascular endothelial edema, decreased mitochondrial damage in neurons, reduced neuronal apoptosis, and a favorable reconstruction of the cerebral vascular network. Additionally, B cell inhibition reduced pro-inflammatory cytokines and immune cells in the brain and peripheral circulation. The immune response alterations observed in the MCAO/R group were consistent with the trends indicated by stroke patient data. Conclusions Temporary inhibition of B-cell activity via aCD19 antibody injection alleviated ischemic brain injury in a mouse model of stroke by suppressing systemic immune reactions. Changes in immune cells within the meninges may play a role, and further investigation is needed to understand the mechanisms involved. These findings suggest that cerebral and systemic immune responses contribute to the pathogenesis of ischemic stroke, and temporary B cell depletion may represent a potential therapeutic target for stroke therapy.

    Keywords: ischemic stroke, B cells, Anti-CD19 antibody, Infalmmation, Menigeal immunity

    Received: 22 Nov 2024; Accepted: 28 Mar 2025.

    Copyright: © 2025 Xu, Peng, Yan, Gao, Zang, Cheng and ZHOU. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: YU ZHOU, Department of Neurosurgery, Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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