Data Entry: Please note that the research database will be replaced by UNIverse by the end of October 2023. Please enter your data into the system https://universe-intern.unibas.ch. Thanks

Login for users with Unibas email account...

Login for registered users without Unibas email account...

 
A Btk transgene restores the antiviral TI-2 antibody responses of xid mice in a dose-dependent fashion
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 3407154
Author(s) Pinschewer, Daniel D.; Ochsenbein, Adrian F.; Satterthwaite, Anne B.; Witte, Owen N.; Hengartner, Hans; Zinkernagel, Rolf M.
Author(s) at UniBasel Pinschewer, Daniel
Year 1999
Title A Btk transgene restores the antiviral TI-2 antibody responses of xid mice in a dose-dependent fashion
Journal European Journal of Immunology
Volume 29
Number 9
Pages / Article-Number 2981-2987
Abstract X-linked agammaglobulinemia in humans and X-linked immunodeficiency (xid) in mice are both caused by mutations in Bruton's tyrosine kinase (Btk). Xid mice lack the early T cell-independent type 2 (TI-2) antibody response to polio virus and to a recombinant vaccinia virus (Vacc-IND-G) expressing the neutralizing determinant of vesicular stomatitis virus (VSV). This response could be restored by introduction of one or two copies of a murine Btk cDNA transgene driven by the Ig heavy chain promoter plus enhancer and depended crucially on a sufficient Btk expression level. Introduction of the same transgene into wild-type mice had little to no negative effect. The TI-1 antibody response to VSV and the T cell-dependent response to lymphocytic choriomeningitis virus were comparable in all mice tested. All mice analyzed eventually reached similar primary and memory antibody titers against all viruses independent of the mouse Btk genotype. These studies show that the xid mutation in mice has no dominant negative effect and that a transgene - even when not provided in the natural genetic context - may be able to restore functional defects resulting from genetic mutation.
Publisher Wiley
ISSN/ISBN 0014-2980 ; 1521-4141
edoc-URL https://edoc.unibas.ch/62021/
Full Text on edoc No
Digital Object Identifier DOI 10.1002/(SICI)1521-4141(199909)29:09<2981::AID-IMMU2981>3.0.CO;2-Y
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/10508272
ISI-Number WOS:000082669900034
Document type (ISI) Article
 
   

MCSS v5.8 PRO. 0.330 sec, queries - 0.000 sec ©Universität Basel  |  Impressum   |    
14/05/2024