Year: 2025
Type: article
Abstract: Description The role of B cells is comparatively understudied in stroke broadly, but particularly in hemorrhagic stroke. There is ample evidence of a B cell response in human stroke patients, and increasing evidence that IgA+ B cells in particular can serve immune regulatory functions in the context of neuroinflammatory diseases broadly. Utilizing a collagenase injection-based murine model of intracerebral hemorrhage (ICH), we report that B cells are robustly recruited to the ipsilateral hemisphere as early as 2 weeks post-ICH, significantly increase by 8 weeks post-ICH, and remain up to 5 months post-ICH. Interestingly, at 8 weeks post-ICH the majority of these cells are IgA+ B cells (85.1% +/- 4.5%; n = 6), suggesting a possible gut origin for these cells. Indeed, single cell sequencing of IgA heavy chains revealed that of 76 clones isolated from 8-week post-ICH brains, 59.6% had matching clonotypes in the small intestine lamina propria, as compared to only 16.8% overlap with splenic B cells. Histological analysis has confirmed the presence of B cells around the hemorrhage site in 8-week post-ICH mouse brains. Finally, spatial sequencing using DBiT-Seq revealed Igha gene expression around the hemorrhage site in ICH but not sham controls. Our findings suggest that intracerebral hemorrhage induces an IgA-specific B cell response within the affected brain hemisphere, underscoring the need to better understand the role IgA+ B cells play in the context of neuroinflammation. Funding Sources Supported by NIH/NINDS 1F31NS132530-01A1 Topic Categories Neuroimmunology (NEUR)
Source: The Journal of Immunology
Institutions: Yale University, Carleton College
Language: English
Subfield: Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W4416451121
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