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                <identifier>oai:data.mendeley.com/cy4mg2gnd3.1</identifier>
                <datestamp>2026-07-14T21:48:14Z</datestamp>
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            <metadata><oai_dc:dc xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
    <dc:creator>Gellrich, Juliane</dc:creator>
    <dc:title>Soraphen A effect on B cells post-stroke</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>Introduction: Immunomodulatory approaches could advance post-stroke therapy. Previous work demonstrated that Soraphen A (SorA) improves functional recovery, in part, by modulating T cell responses. Here, we demonstrate that SorA also directly or indirectly modulates B cell responses.
Methods: Male Nur77GFP mice (12–14 weeks) underwent tMCAO. At reperfusion, mice received intraperitoneal LPS or vehicle; SorA or vehicle was given 2 h later and daily thereafter. B cell activation and differentiation were analyzed by flow cytometry in lungs, spleen, blood, and lymph nodes at 16 h, 2, 3, and 7 d, with GFP indicating antigen-specific activation.
Results: While both SorA and lipopolysaccharide (LPS) replenished splenic B cell numbers depleted by stroke, their effects on B cell subsets diverge. SorA also reversed LPS-induced reductions in lung B cell counts and decreased plasma cell counts. Both treatments increased B cell activation and modulated MHC-II expression. In contrast to T cells, the mode of B cell activation was not affected by SorA treatment. Effects of LPS and SorA on B cell populations were most distinct in the lungs.
Discussion: These findings demonstrate that the beneficial effects of SorA after stroke are not solely mediated by T cell modulation. Further investigation into SorA’s organ-specific impact on different B cell subtypes is crucial to fully elucidate its mechanisms of action.
</dc:description>
    <dc:subject>Immunology</dc:subject>
    <dc:subject>Neurology</dc:subject>
    <dc:subject>Neuroimmunology</dc:subject>
    <dc:subject>Stroke</dc:subject>
    <dc:subject>Ischemic Stroke</dc:subject>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/cy4mg2gnd3.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/cy4mg2gnd3.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
    <dc:rights>http://creativecommons.org/licenses/by/4.0</dc:rights>
    <dc:relation>https://data.mendeley.com/datasets/cy4mg2gnd3</dc:relation>
    <dc:date>2026-07-14T21:48:14Z</dc:date>
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