BCR-dependent lineage plasticity in mature B cells.
Animals
B-Lymphocyte Subsets
/ cytology
Cell Differentiation
/ genetics
Cell Lineage
Cell Plasticity
/ genetics
Immunoglobulin Class Switching
/ genetics
Immunoglobulin Heavy Chains
/ genetics
Immunoglobulin Variable Region
/ genetics
Mice
Mice, Transgenic
Receptors, Antigen, B-Cell
/ genetics
Transcriptome
Journal
Science (New York, N.Y.)
ISSN: 1095-9203
Titre abrégé: Science
Pays: United States
ID NLM: 0404511
Informations de publication
Date de publication:
15 02 2019
15 02 2019
Historique:
received:
22
07
2018
accepted:
17
01
2019
entrez:
16
2
2019
pubmed:
16
2
2019
medline:
2
8
2019
Statut:
ppublish
Résumé
B2 cells engage in classical antibody responses, whereas B1 cells are considered carriers of innate immunity, biased toward recognizing epitopes present on the surfaces of common pathogens and self antigens. To explore the role of B cell antigen receptor (BCR) specificity in driving B1 cell differentiation, we developed a transgenic system allowing us to change BCR specificity in B cells in an inducible and programmed manner. Mature B2 cells differentiated into bona fide B1 cells upon acquisition of a B1 cell-typical self-reactive BCR through a phase of proliferative expansion. Thus, B2 cells have B1 cell differentiation potential in addition to their classical capacity to differentiate into memory and plasma cells, and B1 differentiation can be instructed by BCR-mediated self-reactivity, in the absence of B1-lineage precommitment.
Identifiants
pubmed: 30765568
pii: 363/6428/748
doi: 10.1126/science.aau8475
doi:
Substances chimiques
Immunoglobulin Heavy Chains
0
Immunoglobulin Variable Region
0
Receptors, Antigen, B-Cell
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
748-753Subventions
Organisme : NIAID NIH HHS
ID : R37 AI054636
Pays : United States
Organisme : European Research Council
Pays : International
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.