CD11b^high B Cells Increase after Stroke and Regulate Microglia.

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.