Related Experiment Video
Updated: Jun 17, 2026
09:25
Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM)
Published on: May 8, 2020
A temporal map of B cell diversification mechanisms in mice
Oliver P Skinner1, Saba Asad1, Marcela L Moreira1
1Peter Doherty Institute for Infection and Immunity, Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria, Australia.
Nature Immunology
|June 15, 2026
Summary
During Plasmodium infection, individual B cell clones diversify through isotype switching and somatic hypermutation (SHM). Antimalarial drugs limit B cell responses but do not stop SHM, impacting immunity and protection.
Area of Science:
- Immunology
- Infectious Diseases
- Cell Biology
Background:
- B cell diversification is crucial for adaptive immunity, involving clonal expansion, isotype switching, and somatic hypermutation (SHM).
- Antibody diversity influences malaria immunity through varied antigenic targets, functional classes, and antibody production kinetics.
Purpose of the Study:
- To investigate the temporal dynamics of B cell clone diversification during Plasmodium infection in vivo.
- To elucidate the impact of antimalarial intervention on B cell diversification mechanisms and humoral immune responses.
Main Methods:
- Tracking B cell clone dynamics during Plasmodium infection.
- Analyzing immunoglobulin isotype switching, somatic hypermutation (SHM), and germinal center (GC) formation.
- Assessing the effects of antimalarial intervention on B cell populations and antibody production.
Main Results:
- Individual B cell clones diversify over time during infection, exhibiting isotype variegation and initiating SHM.
- Germinal center (GC) B cells undergo SHM at approximately four mutations per week.
- Antimalarial intervention limits GC size and plasma cell emergence but does not inhibit SHM, affecting antibody levels and protection.
Conclusions:
- Multiple, temporally overlapping mechanisms drive B cell diversification and safeguard humoral immunity during Plasmodium infection.
- B cell development shifts from bone marrow to spleen during infection.
- Antimalarial interventions modulate but do not abolish key B cell diversification processes like SHM.
