| First Author | Yang SH | Year | 2007 |
| Journal | Clin Immunol | Volume | 124 |
| Issue | 3 | Pages | 258-66 |
| PubMed ID | 17662658 | Mgi Jnum | J:123919 |
| Mgi Id | MGI:3719964 | Doi | 10.1016/j.clim.2007.06.003 |
| Citation | Yang SH, et al. (2007) Role of NKT cells in allogeneic islet graft survival. Clin Immunol 124(3):258-66 |
| abstractText | Although NKT cells expressing CD1d-reactive TCR exerted protective role in autoimmune diseases, the regulatory function of CD1d-dependent NKT cells in alloimmune responses has not been investigated thoroughly. Here, we demonstrated the regulatory effects of NKT cells using a pancreas islet transplantation model. CD40/CD154 blocking induced long-term graft survival in most B6 recipients, but B6.CD1d(-/-) recipients showed co-stimulation blockade-resistant rejection. Adoptive transfer of NKT cells into B6.CD1d(-/-) restored tolerizing capacity of co-stimulatory blockade. Activation of NKT cells was effective for the prolongation of graft survival and up-regulated membrane-bound TGF-beta expression transiently on their cell surface. The activated CD1d-dependent NKT cells inhibited alloantigen-driven cell proliferation through cell contacts and the beneficial effect of CD154 blocking for allograft survival was related to TGF-beta pathway. Thus, we can conclude that NKT cells are essential for the stable allograft survival and the regulatory function is dependent on, at least in part, TGF-beta engagement. |
