Related Experiment Video
Updated: Aug 11, 2026
Generation of Human CD40-activated B cells
Published on: October 17, 2009
CD30 is a CD40-inducible molecule that negatively regulates CD40-mediated immunoglobulin class switching in
A Cerutti1, A Schaffer, S Shah
1Department of Pathology, Cornell University Graduate School of Medical Sciences, Cornell University Medical College, New York, New York 10021, USA.
Insights
CD30 coengagement inhibits human B cell differentiation, impacting immunoglobulin class switching. This suggests CD30 plays a critical role in regulating B cell maturation and antibody production.
Area of Science:
- Immunology
- Cell Biology
Background:
- Germinal center B cells undergo maturation and immunoglobulin class switching.
- CD30 is a receptor expressed on activated lymphocytes.
- Understanding CD30's role is crucial for B cell differentiation research.
Purpose of the Study:
- To investigate the role of CD30 in human B cell differentiation using a monoclonal model.
- To determine how CD30 coengagement affects immunoglobulin class switching.
Main Methods:
- Utilized the CL-01 B cell line, a monoclonal model of germinal center maturation.
- Exposed CL-01 cells to CD40L and IL-4 to induce immunoglobulin switching.
- Analyzed the effects of CD30 coengagement on B cell differentiation and gene activation.
Main Results:
- CL-01 B cells, initially IgM+ IgD+ CD30+, switched to IgG, IgA, and IgE upon stimulation.
- CD30 coengagement significantly hampered immunoglobulin class switching.
- CD30 coengagement may interfere with CD40-mediated NF-kappaB signaling.
- Similar CD30-mediated effects were observed in naive human B cells.
Conclusions:
- CD30 critically regulates CD40-mediated differentiation of non-antigen-selected human B cells.
- CD30 signaling influences immunoglobulin class switching and B cell maturation pathways.
- The findings have implications for understanding immune responses and B cell-related disorders.
Abstract:
We used our monoclonal model of germinal center maturation, CL-01 B cells, to investigate the role of CD30 in human B cell differentiation. CL-01 cells are IgM+ IgD+ CD30+ and switch to IgG, IgA, and IgE when exposed to CD40L and IL-4. Switching is hampered by CD30 coengagement, possibly through interference with the CD40-mediated NF-kappaB-dependent transcriptional activation of downstream C(H) genes. The physiological relevance of this phenomenon is emphasized by similar CD30-mediated effects in naive B cells. Expression of CD30 by these cells is induced by CD40L but is inhibited by B cell receptor coengagement and/or exposure to IL-6 and IL-12. Our data suggest that CD30 critically regulates the CD40-mediated differentiation of non-antigen-selected human B cells.
