| First Author | Yadav D | Year | 2009 |
| Journal | Cell Immunol | Volume | 258 |
| Issue | 2 | Pages | 161-71 |
| PubMed ID | 19497561 | Mgi Jnum | J:150136 |
| Mgi Id | MGI:3849781 | Doi | 10.1016/j.cellimm.2009.04.006 |
| Citation | Yadav D, et al. (2009) Altered availability of PD-1/PD ligands is associated with the failure to control autoimmunity in NOD mice. Cell Immunol 258(2):161-71 |
| abstractText | Costimulation via the PD-1 and B7-H1/B7-DC pathway regulates immunity. We investigated whether the PD-1/PD-L pathway is impaired in autoimmune diabetes. A progressive increase in the expression of PD-1 and B7-H1/B7-DC on T cells and APC, respectively, was observed in the pancreatic lymph nodes of female non-obese diabetic (NOD) mice as they developed diabetes. A significantly decreased expression of PD-1 and B7-H1/B7-DC on T cells and APC, respectively, was observed in the periphery of prediabetic NOD mice versus non-diabetic C57BL/6 strain. NOD islets also displayed a reduced capacity to upregulate B7-H1 following exposure to inflammatory cytokines. In vivo blocking studies in NOD/B7-2KONOD mice revealed that B7-H1 and B7-DC positively costimulate autoreactive CD4 and CD8 T cells and may co-operate with B7-2 to augment priming and expansion of naive autoreactive T cells. In summary, these data suggest that diabetes susceptibility in NOD mice is associated with altered PD-1/PD-L availability. |
