Notch 1-deficient common lymphoid precursors adopt a B cell fate in the thymus.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_E47EFFF68EDA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Notch 1-deficient common lymphoid precursors adopt a B cell fate in the thymus.
Périodique
The Journal of experimental medicine
Auteur(s)
Wilson A., MacDonald H.R., Radtke F.
ISSN
0022-1007
Statut éditorial
Publié
Date de publication
2001
Peer-reviewed
Oui
Volume
194
Numéro
7
Pages
1003-1012
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
We have recently reported that Notch 1, a member of the Notch multigene family, is essential for the development of murine T cells. Using a mouse model in which Notch 1 is inactivated in bone marrow (BM) precursors we have shown that B cells instead of T cells are found in the thymus of BM chimeras. However, it is not clear whether these B cells develop by default from a common lymphoid precursor due to the absence of Notch 1 signaling, or whether they arise as a result of perturbed migration of BM-derived B cells and/or altered homeostasis of normal resident thymic B cells. In this report we show that Notch 1-deficient thymic B cells resemble BM B cells in phenotype and turnover kinetics and are located predominantly in the medulla and corticomedullary junction. Peripheral blood lymphocyte analysis shows no evidence of recirculating Notch1(-/)- BM B cells. Furthermore, lack of T cell development is not due to a failure of Notch1(-/)- precursors to home to the thymus, as even after intrathymic reconstitution with BM cells, B cells instead of T cells develop from Notch 1-deficient precursors. Taken together, these results provide evidence for de novo ectopic B cell development in the thymus, and support the hypothesis that in the absence of Notch 1 common lymphoid precursors adopt the default cell fate and develop into B cells instead.
Mots-clé
Animals, B-Lymphocytes/cytology, Bone Marrow Cells, Cell Differentiation, Cell Movement, Hematopoietic Stem Cells/cytology, Membrane Proteins/deficiency, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Receptor, Notch1, Receptors, Cell Surface, Signal Transduction, T-Lymphocytes/cytology, Thymus Gland/cytology, Transcription Factors
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 11:39
Dernière modification de la notice
20/08/2019 16:08
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