Peripheral apoptosis and limited clonal deletion during physiologic murine B lymphocyte development

Mikala JoAnn Simpson, Anna Minh Newen, Christopher McNees, Sukriti Sharma, Dylan Pfannenstiel, Thomas Moyer, David Stephany, Iyadh Douagi, Qiao Wang and Christian Thomas Mayer ()
Additional contact information
Mikala JoAnn Simpson: National Cancer Institute, National Institutes of Health
Anna Minh Newen: National Cancer Institute, National Institutes of Health
Christopher McNees: National Cancer Institute, National Institutes of Health
Sukriti Sharma: National Cancer Institute, National Institutes of Health
Dylan Pfannenstiel: National Cancer Institute, National Institutes of Health
Thomas Moyer: National Institute of Allergy and Infectious Diseases, National Institutes of Health
David Stephany: National Institute of Allergy and Infectious Diseases, National Institutes of Health
Iyadh Douagi: National Institute of Allergy and Infectious Diseases, National Institutes of Health
Qiao Wang: Fudan University
Christian Thomas Mayer: National Cancer Institute, National Institutes of Health

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Self-reactive and polyreactive B cells generated during B cell development are silenced by either apoptosis, clonal deletion, receptor editing or anergy to avoid autoimmunity. The specific contribution of apoptosis to normal B cell development and self-tolerance is incompletely understood. Here, we quantify self-reactivity, polyreactivity and apoptosis during physiologic B lymphocyte development. Self-reactivity and polyreactivity are most abundant in early immature B cells and diminish significantly during maturation within the bone marrow. Minimal apoptosis still occurs at this site, however B cell receptors cloned from apoptotic B cells show comparable self-reactivity to that of viable cells. Apoptosis increases dramatically only following immature B cells leaving the bone marrow sinusoids, but above 90% of cloned apoptotic transitional B cells are not self-reactive/polyreactive. Our data suggests that an apoptosis-independent mechanism, such as receptor editing, removes most self-reactive B cells in the bone marrow. Mechanistically, lack of survival signaling rather than clonal deletion appears to be the underpinning cause of apoptosis in most transitional B cells in the periphery.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-49062-x Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-49062-x

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-49062-x

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().