BCR-dependent lineage plasticity in mature B cells.


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
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

748-753

Subventions

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.

Auteurs

Robin Graf (R)

Immune Regulation and Cancer, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. robin.graf@mdc-berlin.de klaus.rajewsky@mdc-berlin.de.

Jane Seagal (J)

Program in Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.

Kevin L Otipoby (KL)

Program in Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.

Kong-Peng Lam (KP)

Institute for Genetics, University of Cologne, 50674 Cologne, Germany.

Salah Ayoub (S)

Systems Biology of Gene Regulatory Elements, Max Delbrück Center for Molecular Medicine in the Helmholtz Association Berlin, 13125 Berlin, Germany.

Baochun Zhang (B)

Program in Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.

Sandrine Sander (S)

Immune Regulation and Cancer, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
Adaptive Immunity and Lymphoma, German Cancer Research Center / National Center for Tumor Diseases Heidelberg, 69120 Heidelberg, Germany.

Van Trung Chu (VT)

Immune Regulation and Cancer, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
Berlin Institute of Health, 10117 Berlin, Germany.

Klaus Rajewsky (K)

Immune Regulation and Cancer, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany. robin.graf@mdc-berlin.de klaus.rajewsky@mdc-berlin.de.
Program in Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.
Institute for Genetics, University of Cologne, 50674 Cologne, Germany.

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Classifications MeSH