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Specific Induction of Double Negative B Cells During Protective and Pathogenic Immune Responses
Christoph Ruschil1,2, Gisela Gabernet3, Gildas Lepennetier4
1Department of Neurology and Stroke, Eberhard-Karls University, Tübingen, Germany.
Frontiers in Immunology
|January 4, 2021
Summary
Double negative (DN) B cells expand in autoimmune diseases and after vaccination. These cells show clonal expansion and respond to antigens, suggesting a role in immune responses.
Area of Science:
- Immunology
- Cell Biology
Background:
- Double negative (DN) B cells (CD19+CD20lowCD27-IgD-) are increased in autoimmune and infectious diseases.
- The precise function of DN B cells in humoral immunity is not fully understood.
Purpose of the Study:
- To investigate the role and characteristics of DN B cells in inflammatory conditions and response to vaccination.
- To determine if DN B cells are antigen-specific and clonally expanded.
Main Methods:
- Systematic flow cytometry of peripheral blood B cell subsets.
- Transcriptome analysis of DN B cells.
- Immunoglobulin VH transcriptome sequencing and recombinant antibody analysis.
Main Results:
- DN B cells were expanded in patients with myasthenia gravis, Guillain-Barré syndrome, neuromyelitis optica spectrum disorder, meningitis/encephalitis, and rheumatic disorders.
- DN B cells were induced in healthy subjects after influenza and tick-borne encephalitis virus vaccination.
- Transcriptome analysis showed DN B cell gene expression similar to naive B cells, memory B cells, and plasmablasts.
- DN B cells demonstrated clonal expansion and targeted the vaccine antigen, indicating antigen specificity.
Conclusions:
- DN B cells are expanded in various inflammatory neurologic diseases.
- DN B cells represent an inducible B cell population responding to antigenic stimulation.
- DN B cells may mature through an extra-follicular pathway.
Keywords:
B cellsTBE vaccinationautoimmune disordersdouble negative B cellsinfluenza vaccinationneuromyelitis optica spectrum disordervaccinationMore Related Videos
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