Related Experiment Video
Updated: Jun 25, 2026
Co-Culture In Vitro Systems to Reproduce the Cancer-Immunity Cycle
Published on: June 7, 2024
CD98hc facilitates B cell proliferation and adaptive humoral immunity
Joseph Cantor1, Cecille D Browne, Raphael Ruppert
1Department of Medicine, University of California San Diego, La Jolla, USA.
Insights
The heavy chain of CD98 (CD98hc) is crucial for B cell proliferation and antibody production in adaptive immunity. Its absence halts B cell growth, impacting immune responses.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Adaptive immunity relies on lymphocyte proliferation and clonal expansion.
- The heavy chain of CD98 (CD98hc) is a transmembrane protein involved in cell signaling and transport.
Purpose of the Study:
- To investigate the role of CD98hc in B cell proliferation and antibody responses.
- To determine the specific functions of CD98hc required for B cell activation and expansion.
Main Methods:
- Generating B cell-specific CD98hc knockout mice.
- Analyzing B cell activation, proliferation, and antibody production.
- Utilizing CD98hc mutants to assess functional domains.
Main Results:
- B cell-specific deletion of CD98hc suppressed B cell proliferation and plasma cell formation, leading to reduced antibody responses.
- CD98hc deficiency impaired later Erk1/2 activation and p27 downregulation but not early B cell activation.
- The integrin-binding domain of CD98hc, not its amino acid transport function, was essential for B cell proliferation.
Conclusions:
- CD98hc is critical for integrin-dependent B cell proliferation, supporting adaptive immune responses.
- The findings suggest CD98hc plays a vital role in vertebrate adaptive immunity evolution.
Abstract:
The proliferation of antigen-specific lymphocytes and resulting clonal expansion are essential for adaptive immunity. We report here that B cell-specific deletion of the heavy chain of CD98 (CD98hc) resulted in lower antibody responses due to total suppression of B cell proliferation and subsequent plasma cell formation. Deletion of CD98hc did not impair early B cell activation but did inhibit later activation of the mitogen-activated protein kinase Erk1/2 and downregulation of the cell cycle inhibitor p27. Reconstitution of CD98hc-deficient B cells with CD98hc mutants showed that the integrin-binding domain of CD98hc was required for B cell proliferation but that the amino acid-transport function of CD98hc was dispensable for this. Thus, CD98hc supports integrin-dependent rapid proliferation of B cells. We propose that the advantage of adaptive immunity favored the appearance of CD98hc in vertebrates.
More Related Videos
Related Concept Videos
01:22T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
01:24B Cell Activation and Differentiation
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
01:26Antigens Involved in Adaptive Immunity
Complete Antigens
Complete antigens possess both immunogenicity and reactivity.
01:40Cell-mediated Immune Responses
01:23Cells of the Adaptive Immune Response
01:20Special Features of Adaptive Immunity
The primary cell types involved in adaptive immunity are T cells and B cells. Each type has a unique role in defending the body against pathogens. T cells are responsible for cell-mediated immunity. They identify and eliminate infected cells directly,...