scholarly journals Germline TRAV5D-4 T-Cell Receptor Sequence Targets a Primary Insulin Peptide of NOD Mice

Diabetes ◽  
2012 ◽  
Vol 61 (4) ◽  
pp. 857-865 ◽  
Author(s):  
M. Nakayama ◽  
T. Castoe ◽  
T. Sosinowski ◽  
X. He ◽  
K. Johnson ◽  
...  
1991 ◽  
Vol 21 (5) ◽  
pp. 1163-1169 ◽  
Author(s):  
Pascal Sempé ◽  
Pierre Bédossa ◽  
Marie-Francoise Richard ◽  
Maria-Carme Villà ◽  
Jean-Francois Bach ◽  
...  

1996 ◽  
Vol 184 (5) ◽  
pp. 1755-1768 ◽  
Author(s):  
U McKeever ◽  
S Khandekar ◽  
J Newcomb ◽  
J Naylor ◽  
P Gregory ◽  
...  

The BDC 2.5 T cell clone is specific for pancreatic beta-cell antigen presented by I-Ag7, and greatly accelerates diabetes when injected into 10-21-d-old nonobese diabetic (NOD) mice. The BDC 2.5 T cell receptor (TCR) has been solubilized as a TCR-IgG1 chimeric protein. All NOD mice immunized against BDC 2.5 TCR-IgG1 produced antibodies recognizing TCR C alpha/C beta epitopes that were inaccessible on the T cell surface. 56% of the mice produced antibodies against the BDC 2.5 clonotype that specifically blocked antigen activation of BDC 2.5 cells. We have used the adoptive transfer model of diabetes to demonstrate that maternal immunization with soluble TCR protects young mice from diabetes induced by the BDC 2.5 T cell clone.


1993 ◽  
Vol 6 (4) ◽  
pp. 405-422 ◽  
Author(s):  
Peter Berschick ◽  
Karin Fehsel ◽  
Hans Ulrich Weltzien ◽  
Hubert Kolb

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e52054 ◽  
Author(s):  
Ramiro Diz ◽  
Alaina Garland ◽  
Benjamin G. Vincent ◽  
Mark C. Johnson ◽  
Nicholas Spidale ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112467 ◽  
Author(s):  
Joanna Kern ◽  
Robert Drutel ◽  
Silvia Leanhart ◽  
Marek Bogacz ◽  
Rafal Pacholczyk

Diabetes ◽  
1999 ◽  
Vol 48 (1) ◽  
pp. 34-42 ◽  
Author(s):  
H. S. Jun ◽  
P. Santamaria ◽  
H. W. Lim ◽  
M. L. Zhang ◽  
J. W. Yoon

1991 ◽  
Vol 173 (5) ◽  
pp. 1091-1097 ◽  
Author(s):  
N Nakano ◽  
H Kikutani ◽  
H Nishimoto ◽  
T Kishimoto

Five islet-reactive T cell clones were established from islet-infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V beta 16. The expression of V beta 16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V beta 16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis.


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