Redundant functions of TCF-1 and LEF-1 during T and NK cell development, but unique role of TCF-1 for Ly49 NK cell receptor acquisition.
Details
Serval ID
serval:BIB_FB20A05E1494
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Redundant functions of TCF-1 and LEF-1 during T and NK cell development, but unique role of TCF-1 for Ly49 NK cell receptor acquisition.
Journal
European journal of immunology
ISSN
0014-2980
Publication state
Published
Issued date
2003
Peer-reviewed
Oui
Volume
33
Number
5
Pages
1393-1398
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
Members of the TCF/LEF (T cell factor / lymphoid enhancer factor) family of DNA-binding factors play important roles during embryogenesis, the establishment and/or maintenance of self-renewing tissues such as the immune system and for malignant transformation. Specifically, it has been shown that TCF-1 is required for T cell development. A role for LEF-1 became apparent when mice harbored two hypomorphic TCF-1 alleles and consequently expressed low levels of TCF-1. Here we show that NK cell development is similarly regulated by redundant functions of TCF-1 and LEF-1, whereby TCF-1 contributes significantly more to NK cell development than LEF-1. Despite this role for NK cell development, LEF-1 is not required for the establishment of a repertoire of MHC class I-specific Ly49 receptors on NK cells. The proper formation of this repertoire depends to a large extent on TCF-1. These findings suggest common and distinct functions of TCF-1 and LEF-1 during lymphocyte development.
Keywords
Animals, Antigens, Ly/analysis, DNA-Binding Proteins/physiology, Killer Cells, Natural/physiology, Lectins, C-Type, Lymphoid Enhancer-Binding Factor 1, Mice, Mice, Inbred C57BL, Receptors, NK Cell Lectin-Like, T Cell Transcription Factor 1, T-Lymphocytes/physiology, Transcription Factors/physiology
Pubmed
Web of science
Open Access
Yes
Create date
17/01/2008 15:24
Last modification date
20/08/2019 16:26