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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
Acute ischaemic stroke alters the composition and function of circulating B cells
Mehwish Younas1, Harry R Deijnen2, Ruth Stephens3
1Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK; Division of Neuroscience, The University of Manchester, Manchester, UK; Geoffrey Jefferson Brain Research Centre, Manchester Academic Health Science Centre, Northern Care Alliance NHS Foundation Trust, University of Manchester, Manchester, UK; Present address: Functional Genomics, Centre of Genomics Research, Discovery Sciences, AstraZeneca, Cambridge, UK.
Acute ischaemic stroke (AIS) alters circulating B cells, reducing innate-like marginal zone B cells and impairing their function. Neuroimmune factors, like noradrenaline, drive these changes, impacting immune response post-stroke.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Circulating B cells, including innate-like populations, play key roles in immunity.
- The impact of tissue injury, particularly acute ischaemic stroke (AIS), on B cell function is not well understood.
- AIS is a major cause of neurological disability and is linked to systemic immune dysfunction.
Purpose of the Study:
- To investigate the effects of AIS on circulating B cell populations and their functionality.
- To explore the role of neuroimmune factors in modulating B cell responses after stroke.
- To determine if stroke or secondary infections are the primary drivers of observed B cell alterations.
Main Methods:
- Analysis of circulating B cell populations in AIS patients and controls.
- Functional assays of B cells, including cytokine and immunoglobulin release.
- Investigation of B cell adrenergic receptor expression and response to noradrenaline (NA).
- In vitro experiments exposing healthy B cells to NA.
Main Results:
- AIS patients showed reduced numbers of marginal zone (MZ)-like B cells, an innate-like subset.
- B cells from AIS patients exhibited impaired release of Immunoglobulin M (IgM) and regulatory cytokines (IL-6, IL-10).
- B cells express adrenergic receptors, and in vitro exposure to NA mimicked some AIS-related functional changes, including increased MZ-like B cell death.
- Observed B cell alterations were primarily attributed to the stroke itself, not secondary infections.
Conclusions:
- Acute ischaemic stroke rapidly modifies circulating B cell populations and their function.
- Neuroimmune signaling, particularly via noradrenaline, significantly impacts B cell responses post-stroke.
- Altered innate-like B cell function is a previously unrecognized feature of the systemic immune response to AIS.
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