ArticleJournal of neuroinflammation2026
BTLA-mediated regulation of neuroimmune responses enhances recovery after intracerebral hemorrhage.
Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundModulating harmful neuroimmune responses is a promising therapeutic approach for hemorrhagic stroke, a condition that still lacks effective treatment. The immune checkpoint B and T Lymphocyte Attenuator (BTLA) helps suppress immune activation; however, its role in intracerebral hemorrhage (ICH) remains unclear. This study explores whether a BTLA-activating antibody can reduce neuroinflammation, mitigate brain injury, improve recovery after ICH, and elucidate the underlying mechanisms.
methodsAn ICH model was generated in male C57BL/6 mice by stereotactic injection of collagenase VII-S into the left striatum. The mice received intraperitoneal administration of an agonistic anti-BTLA antibody to serve as a BTLA agonist. Therapeutic effects were evaluated using a multimodal approach that included flow cytometry, Western blotting, immunofluorescence staining, histological examination, and behavioral tests. Additionally, microglial depletion was performed by feeding the CSF1R inhibitor PLX5622.
resultsOur findings demonstrate that a single dose of an agonistic anti-BTLA antibody, administered 30 min post-ICH, significantly reduced the infiltration of CD45
conclusionThe agonistic anti-BTLA antibody significantly attenuates neuroinflammation and reduces brain injury following ICH, accompanied by enhanced neurological recovery. This protective effect appears to be mediated through microglia-dependent mechanisms. Our findings highlight BTLA may be a novel and promising immunomodulatory target for the treatment of ICH.
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