CD11b B Cells Increase after Stroke and Regulate Microglia

Janelle M. Korf, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Pedram Honarpisheh, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Eric C. Mohan, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Anik Banerjee, University of Texas MD Anderson Cancer Center, UTHealth Graduate School of Biomedical Sciences, Houston, TX.
Maria P. Blasco-Conesa, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Parisa Honarpisheh, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Gary U. Guzman, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Romeesa Khan, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Bhanu P. Ganesh, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Amy L. Hazen, University of Texas McGovern Medical School, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, Houston, TX.
Juneyoung Lee, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Aditya Kumar, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Louise D. McCullough, Department of Neurology, University of Texas McGovern Medical School, Houston, TX.
Anjali Chauhan, Department of Neurology, University of Texas McGovern Medical School, Houston, TX; anjali.chauhan@uth.tmc.edu.

Document Type

Article

Abstract

Recent studies have highlighted the deleterious contributions of B cells to post-stroke recovery and cognitive decline. Different B cell subsets have been proposed on the basis of expression levels of transcription factors (e.g., T-bet) as well as specific surface proteins. CD11b (α-chain of integrin) is expressed by several immune cell types and is involved in regulation of cell motility, phagocytosis, and other essential functions of host immunity. Although B cells express CD11b, the CD11b subset of B cells has not been well characterized, especially in immune dysregulation seen with aging and after stroke. Here, we investigate the role of CD11b B cells in immune responses after stroke in young and aged mice. We evaluated the ability of CD11b B cells to influence pro- and anti-inflammatory phenotypes of young and aged microglia (MG). We hypothesized that CD11b B cells accumulate in the brain and contribute to neuroinflammation in aging and after stroke. We found that CD11b B cells are a heterogeneous subpopulation of B cells predominantly present in naive aged mice. Their frequency increases in the brain after stroke in young and aged mice. Importantly, CD11b B cells regulate MG phenotype and increase MG phagocytosis in both ex vivo and in vivo settings, likely by production of regulatory cytokines (e.g., TNF-α). As both APCs and adaptive immune cells with long-term memory function, B cells are uniquely positioned to regulate acute and chronic phases of the post-stroke immune response, and their influence is subset specific.

Medical Subject Headings

Animals; B-Lymphocytes (metabolism); CD11b Antigen (metabolism); Cell Count; Cytokines (metabolism); Mice; Mice, Inbred C57BL; Microglia (metabolism); Stroke (metabolism)

Publication Date

7-15-2022

Publication Title

Journal of immunology (Baltimore, Md. : 1950)

E-ISSN

1550-6606

Volume

209

Issue

2

First Page

288

Last Page

300

PubMed ID

35732342

Digital Object Identifier (DOI)

10.4049/jimmunol.2100884

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