Authors
Moncef Zouali
Published in
The European journal of neuroscience. Volume 64. Issue 7. Pages e70707.
Abstract
Whereas the pathobiology of stroke is traditionally thought to be mediated mainly by innate immune cells, the recent discovery that immune tolerance to brain-specific antigens takes place in the meninges suggests that the CNS makes use of unique pathways to respond to brain-derived antigens. By virtue of their adaptive and innate-like functions, B lymphocytes can play multiple roles in stroke. Following acute ischemic stroke, B cells home to the site of injury and produce cytokines that can either promote or exacerbate inflammation. They also secrete autoantibodies against neuronal and/or vascular components, potentially aggravating the damage and contributing to long-term neurological deficits. Clinical studies indicate that stroke patients can develop B-cell responses that potentially contribute to dementia. In animal models, age-associated B cells were found to worsen inflammation and contribute to autoimmunity. Through the production of antibodies and cytokines, B cells play a role in affecting the permeability of the blood-brain barrier, thereby compromising its integrity. In addition to contributing to adverse outcomes by enhancing inflammation and producing harmful autoantibodies, B cells have been demonstrated to exhibit protective effects, helping to resolve inflammation and promoting tissue repair. In mice, the absence of B cells results in delayed recovery, suggesting that B-cell migration to different regions of the brain imparts reduction of poststroke cognitive impairment. Gaining further insight into the multiple roles of B cells in stroke could lead to the development of novel therapeutic strategies and biomarker development.
PMID:
42855877
Bibliographic data and abstract were imported from PubMed on 10 Oct 2026.
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