Does B lymphocyte-mediated autoimmunity contribute to post-stroke dementia?

Does B lymphocyte-mediated autoimmunity contribute to post-stroke dementia?
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DOI:
10.1016/j.bbi.2016.08.009
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发表时间:
2017-08
期刊:
Brain, behavior, and immunity
影响因子:
--
通讯作者:
Buckwalter MS
Buckwalter MS
中科院分区:
其他
文献类型:
--
作者:
Doyle KP;Buckwalter MS

文献摘要

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中风后认知能力下降和痴呆是一个严重的公共卫生问题,30%的中风幸存者患有痴呆症。这种高流行率的原因尚不清楚。致病性B细胞对受损CNS的反应是一个可能的促成因素。B淋巴细胞和抗体存在于一些死于中风和痴呆的人类受试者的中风核心中和周围,并且在中风后发展延迟性认知功能障碍的小鼠在中风病变中具有B淋巴细胞簇,并且在中风半球中具有抗体浸润。B淋巴细胞的消融可预防小鼠中风后认知障碍。针对B细胞的多种药物是FDA批准的,因此如果在中风患者的子集中发生致病性B细胞反应,这是潜在的可治疗的。然而,也已经证明调节性B细胞在中风的小鼠模型中是有益的。因此,重要的是要了解B淋巴细胞对恢复与致病性的相对贡献,以及这种平衡在不同个体中是否是异质的。因此,本综述的目的是总结目前的知识状态方面的作用,B淋巴细胞在脑卒中后痴呆的病因。
Post-stroke cognitive decline and dementia pose a significant public health problem, with 30% of stroke survivors suffering from dementia. The reason for this high prevalence is not well understood. Pathogenic B cell responses to the damaged CNS are one possible contributing factor. B-lymphocytes and antibodies are present in and around the stroke core of some human subjects who die with stroke and dementia, and mice that develop delayed cognitive dysfunction after stroke have clusters of B-lymphocytes in the stroke lesion, and antibody infiltration in the stroked hemisphere. The ablation of B-lymphocytes prevents post-stroke cognitive impairment in mice. Multiple drugs that target B cells are FDA approved, and so if pathogenic B cell responses are occurring in a subset of stroke patients, this is potentially treatable. However, it has also been demonstrated that regulatory B cells can be beneficial in mouse models of stroke. Consequently, it is important to understand the relative contribution of B-lymphocytes to recovery versus pathogenicity, and if this balance is heterogeneous in different individuals. Therefore, the purpose of this review is to summarize the current state of knowledge with regard to the role of B-lymphocytes in the etiology of post-stroke dementia.