| First Author | Bolinger B | Year | 2008 |
| Journal | Blood | Volume | 111 |
| Issue | 9 | Pages | 4588-95 |
| PubMed ID | 18195091 | Mgi Jnum | J:134363 |
| Mgi Id | MGI:3785364 | Doi | 10.1182/blood-2007-09-114769 |
| Citation | Bolinger B, et al. (2008) Immunologic ignorance of vascular endothelial cells expressing minor histocompatibility antigen. Blood 111(9):4588-95 |
| abstractText | Endothelial cells (ECs) presenting minor histocompatibility antigen (mhAg) are major target cells for alloreactive effector CD8(+) T cells during chronic transplant rejection and graft-versus-host disease (GVHD). The contribution of ECs to T-cell activation, however, is still a controversial issue. In this study, we have assessed the antigen-presenting capacity of ECs in vivo using a transgenic mouse model with beta-galactosidase (beta-gal) expression confined to the vascular endothelium (Tie2-LacZ mice). In a GVHD-like setting with adoptive transfer of beta-gal-specific T-cell receptor-transgenic T cells, beta-gal expression by ECs was not sufficient to either activate or tolerize CD8(+) T cells. Likewise, transplantation of fully vascularized heart or liver grafts from Tie2-LacZ mice into nontransgenic recipients did not suffice to activate beta-gal-specific CD8(+) T cells, indicating that CD8(+) T-cell responses against mhAg cannot be initiated by ECs. Moreover, we could show that spontaneous activation of beta-gal-specific CD8(+) T cells in Tie2-LacZ mice was exclusively dependent on CD11c(+) dendritic cells (DCs), demonstrating that mhAgs presented by ECs remain immunologically ignored unless presentation by DCs is granted. |
