Abrogation of the Allelic Exclusion in a T Cell Receptor β Chain Gene Transgenic Mouse Strain

1995 ◽  
Vol 24 (6) ◽  
pp. 927-946 ◽  
Author(s):  
O. Mazda ◽  
Y. Aiba ◽  
N. Hattori ◽  
M. Li ◽  
S. Fujimoto ◽  
...  
1995 ◽  
Vol 42 (4) ◽  
pp. 331-339 ◽  
Author(s):  
Antoine Alam ◽  
Jacqueline Lulé ◽  
Héléne Coppin ◽  
Nathalie Lambert ◽  
Bernard Maziéres ◽  
...  

2002 ◽  
Vol 119 (2) ◽  
pp. 377-383 ◽  
Author(s):  
Achim K. Moesta ◽  
Animesh A. Sinha ◽  
Mong-Shang Lin ◽  
Luis A. Diaz

1998 ◽  
Vol 187 (1) ◽  
pp. 105-116 ◽  
Author(s):  
Laurence Ardouin ◽  
Jamila Ismaili ◽  
Bernard Malissen ◽  
Marie Malissen

The pre–T cell receptor (TCR) associates with CD3-transducing subunits and triggers the selective expansion and maturation of T cell precursors expressing a TCR-β chain. Recent experiments in pre-Tα chain-deficient mice have suggested that the pre-TCR may not be required for signaling allelic exclusion at the TCR-β locus. Using CD3-ε– and CD3-ζ/η–deficient mice harboring a productively rearranged TCR-β transgene, we showed that the CD3-γδε and CD3-ζ/η modules, and by inference the pre-TCR/CD3 complex, are each essential for the establishment of allelic exclusion at the endogenous TCR-β locus. Furthermore, using mutant mice lacking both the CD3-ε and CD3-ζ/η genes, we established that the CD3 gene products are dispensable for the onset of V to (D)J recombination (V, variable; D, diversity; J, joining) at the TCR-β, TCR-γ, and TCR-δ loci. Thus, the CD3 components are differentially involved in the sequential events that make the TCR-β locus first accessible to, and later insulated from, the action of the V(D)J recombinase.


Nature ◽  
1986 ◽  
Vol 322 (6077) ◽  
pp. 376-378 ◽  
Author(s):  
Ute Hochgeschwender ◽  
Hans Ulrich Weltzien ◽  
Klaus Eichmann ◽  
R. Bruce Wallace ◽  
Jörg T. Epplen

Sign in / Sign up

Export Citation Format

Share Document