Eur J Neurosci. 2026 Oct;64(7):e70707. doi: 10.1111/ejn.70707.
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 | DOI:10.1111/ejn.70707