|  Help  |  About  |  Contact Us

Publication : A mechanism for the major histocompatibility complex-linked resistance to autoimmunity.

First Author  Schmidt D Year  1997
Journal  J Exp Med Volume  186
Issue  7 Pages  1059-75
PubMed ID  9314555 Mgi Jnum  J:108768
Mgi Id  MGI:3624873 Doi  10.1084/jem.186.7.1059
Citation  Schmidt D, et al. (1997) A mechanism for the major histocompatibility complex-linked resistance to autoimmunity. J Exp Med 186(7):1059-75
abstractText  Certain major histocompatibility complex (MHC) class II haplotypes encode elements providing either susceptibility or dominant resistance to the development of spontaneous autoimmune diseases via mechanisms that remain undefined. Here we show that a pancreatic beta cell-reactive, I-Ag7-restricted, transgenic TCR that is highly diabetogenic in nonobese diabetic mice (H-2(g7)) undergoes thymocyte negative selection in diabetes-resistant H-2(g7/b), H-2(g7/k), H-2(g7/q), and H-2(g7/nb1) NOD mice by engaging antidiabetogenic MHC class II molecules on thymic bone marrow-derived cells, independently of endogenous superantigens. Thymocyte deletion is complete in the presence of I-Ab, I-Ak + I-Ek or I-Anb1 + I-Enb1 molecules, partial in the presence of I-Aq or I-Ak molecules alone, and absent in the presence of I-As molecules. Mice that delete the transgenic TCR develop variable degrees of insulitis that correlate with the extent of thymocyte deletion, but are invariably resistant to diabetes development. These results provide an explanation as to how protective MHC class II genes carried on one haplotype can override the genetic susceptibility to an autoimmune disease provided by allelic MHC class II genes carried on a second haplotype.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

12 Bio Entities

Trail: Publication

0 Expression