Abstract
Abstract Stroke is one of the leading causes of mortality and morbidity worldwide. Upon cerebral ischemia, an inflammatory reaction takes place in the brain. Infiltration of different immune cell subsets as well as activation of resident microglia cells have been shown to have both beneficial and detrimental effects on stroke outcome. For a long time, research in the field of adaptive immunity after stroke has mostly focused on T lymphocytes and only recently, several publications shed light on the importance of B lymphocytes in the acute and chronic phases of ischemic stroke. In this review, we will focus on the role of B cells in the ischemic brain and describe possible antibody-dependent and antibody-independent mechanisms in the development of post-stroke cognitive deficits.
Highlights
Stroke is one of the leading causes of mortality and morbidity worldwide
Lymphocytic apoptosis and dysfunction induced by an over-activation of the sympathetic nervous system (Prass et al, 2003) and anti-inflammatory effects on the innate immune system mediated by parasympathetic, cholinergic pathways (Engel et al, 2015) are involved in the pathogenesis of this temporary failure of host defense
marginal zone (MZ) B cells are innate-like immune cells rapidly producing immunoglubulin (Ig) M upon inflam
Summary
Stroke is one of the leading causes of mortality and morbidity worldwide. Upon cerebral ischemia, an inflammatory reaction takes place in the brain. We will focus on the role of B cells in the ischemic brain and describe possible antibody-dependent and antibody-independent mechanisms in the development of post-stroke cognitive deficits. A key mechanism facilitating SAP is stroke-induced immune depression (Chamorro et al, 2012; Iadecola and Anrather, 2011a; Meisel et al, 2005; Westendorp et al, 2011). Lymphocytic apoptosis and dysfunction induced by an over-activation of the sympathetic nervous system (Prass et al, 2003) and anti-inflammatory effects on the innate immune system mediated by parasympathetic, cholinergic pathways (Engel et al, 2015) are involved in the pathogenesis of this temporary failure of host defense. – B cells in stroke matory challenge
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