Genetic loss of NFAT2 (NFATc1) impairs B cell development of B1 and B2 B cells.
Animals
Antigens, Differentiation, B-Lymphocyte
/ analysis
B-Lymphocyte Subsets
/ cytology
Female
Gene Expression Regulation, Developmental
Gene Knockout Techniques
Genes, Lethal
Heterozygote
Immunoglobulin D
/ biosynthesis
Immunoglobulin M
/ biosynthesis
Leukocyte Common Antigens
/ biosynthesis
Lymphocyte Activation
Lymphoid Tissue
/ growth & development
Lymphopoiesis
/ genetics
Male
Mice
Mice, Inbred C57BL
NFATC Transcription Factors
/ deficiency
Organ Specificity
Specific Pathogen-Free Organisms
B1 B cells
Conditional knock out mice
Development
Follicular B cells
NFAT2
NFATc1
Proliferation
Transitional B cells
Journal
Cellular immunology
ISSN: 1090-2163
Titre abrégé: Cell Immunol
Pays: Netherlands
ID NLM: 1246405
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
27
11
2019
revised:
18
01
2020
accepted:
25
01
2020
pubmed:
6
2
2020
medline:
18
8
2020
entrez:
5
2
2020
Statut:
ppublish
Résumé
NFAT2 activity was shown to be of critical importance in B cell receptor signaling, development and proliferation; however its role in B cell development in the periphery is still not completely understood. We confirmed that NFAT2 deletion leads to impaired B1 B cell development, supported by our finding of limited B1 progenitors in the bone marrow and spleen of NFAT2 deficient mice. Moreover, we show for the first time that loss of NFAT2 increases immature B cells in particular transitional T2 and T3 as well as mature follicular B cells while marginal zone B cells are decreased. We further demonstrate that NFAT2 regulates the expression of B220, CD23, CD38, IgM/IgD and ZAP70 in murine B cells. In vivo analyses revealed decreased proliferation and increased apoptosis of NFAT2 deficient B cells. In summary, this study provides an extensive analysis of the role of NFAT2 in peripheral B lymphocyte development.
Identifiants
pubmed: 32014271
pii: S0008-8749(19)30505-2
doi: 10.1016/j.cellimm.2020.104048
pii:
doi:
Substances chimiques
Antigens, Differentiation, B-Lymphocyte
0
Immunoglobulin D
0
Immunoglobulin M
0
NFATC Transcription Factors
0
Nfatc1 protein, mouse
0
Leukocyte Common Antigens
EC 3.1.3.48
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
104048Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.