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Updated: Sep 7, 2025

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
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CD11bhigh B Cells Increase after Stroke and Regulate Microglia.

Janelle M Korf1,2, Pedram Honarpisheh1,2, Eric C Mohan1

  • 1Department of Neurology, University of Texas McGovern Medical School, Houston, TX.

Journal of Immunology (Baltimore, Md. : 1950)
|June 22, 2022
PubMed
Summary

CD11b-high B cells accumulate in the brain after stroke, influencing microglia and potentially impairing recovery. This subset, more prevalent in aged mice, plays a role in neuroinflammation and immune responses post-stroke.

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Area of Science:

  • Neuroimmunology
  • Stroke Pathophysiology
  • Innate and Adaptive Immunity

Background:

  • B cells impact post-stroke recovery and cognitive function.
  • B cell subsets are defined by transcription factors and surface proteins.
  • CD11b is crucial for immune cell functions, but CD11b-high B cells remain poorly understood, especially in aging and stroke contexts.

Purpose of the Study:

  • Investigate the role of CD11b-high B cells in immune responses following stroke in young and aged mice.
  • Evaluate the influence of CD11b-high B cells on microglial phenotypes and phagocytosis.
  • Test the hypothesis that CD11b-high B cells accumulate in the brain and contribute to neuroinflammation.

Main Methods:

  • Analysis of CD11b-high B cell frequency in naive and post-stroke young and aged mice.
  • Evaluation of CD11b-high B cells' effect on microglial (MG) pro- and anti-inflammatory phenotypes ex vivo and in vivo.
  • Assessment of microglial phagocytosis modulated by CD11b-high B cells.

Main Results:

  • CD11b-high B cells represent a heterogeneous subpopulation, more frequent in naive aged mice.
  • Stroke increases the frequency of CD11b-high B cells in the brain of both young and aged mice.
  • CD11b-high B cells modulate MG phenotype and enhance MG phagocytosis, potentially via cytokine production (e.g., TNF-α).

Conclusions:

  • CD11b-high B cells are present in the brain and their frequency increases post-stroke.
  • These cells influence microglial function and phagocytosis, contributing to neuroinflammation.
  • Subset-specific B cell functions are critical for regulating the immune response during acute and chronic stroke phases.