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In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
Published on: January 20, 2019
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Abatacept modulates CD80 and CD86 expression and memory formation in human B-cells
Raquel Lorenzetti1, Iga Janowska1, Cristian Roberto Smulski2
1Department of Rheumatology and Clinical Immunology, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Baden-Württemberg, 79106, Germany.
Journal of Autoimmunity
|May 6, 2019
Summary
Abatacept directly reduces B-cell CD80/CD86 expression, impacting antigen presentation and T-cell activation. This study reveals a new therapeutic mechanism for abatacept in B-cell mediated autoimmune diseases like rheumatoid arthritis.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Cytotoxic T lymphocyte antigen-4 (CTLA-4) regulates T-cell activation and is found on T-regulatory cells.
- Abatacept (CTLA-4 Ig) treats rheumatoid arthritis (RA) by affecting T-cells, modulating CD80/CD86 on antigen-presenting cells (APCs).
- B-cells express CD80/CD86 and act as APCs, suggesting they may be a direct target of abatacept.
Purpose of the Study:
- Investigate abatacept's direct effects on human B-lymphocytes in vitro.
- Assess abatacept's impact on B-cells in patients with rheumatoid arthritis.
Main Methods:
- Studied the effect of abatacept on healthy donor B-cell phenotype, activation, and CD80/CD86 expression in vitro.
- Monitored nine abatacept-treated RA patients for treatment response, immunoglobulin levels, autoantibodies (ACPA, RF), B-cell phenotype, and ACPA-specific switched memory B-cell frequency.
Main Results:
- Abatacept did not affect B-cell development but dose-dependently decreased CD80/CD86 expression on B-cells via internalization.
- RA patients showed decreased plasmablasts and serum IgG, moderate ACPA-titer decline, and a significant decrease in ACPA-specific switched memory B-cells.
Conclusions:
- Abatacept directly targets B-cells by reducing CD80/CD86 expression.
- This mechanism may impair antigen presentation and T-cell activation, leading to altered B-cell selection.
- Provides a new therapeutic insight for abatacept in treating B-cell mediated autoimmune conditions.
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