| First Author | Arancibia-Cárcamo CV | Year | 2004 |
| Journal | Eur J Immunol | Volume | 34 |
| Issue | 2 | Pages | 471-80 |
| PubMed ID | 14768052 | Mgi Jnum | J:115470 |
| Mgi Id | MGI:3691749 | Doi | 10.1002/eji.200324195 |
| Citation | Arancibia-Carcamo CV, et al. (2004) A CIITA-independent pathway that promotes expression of endogenous rather than exogenous peptides in immune-privileged sites. Eur J Immunol 34(2):471-80 |
| abstractText | A CIITA-independent pathway of MHC class II expression has been found in the eye and the brain, both immune-privileged sites. Although corneal endothelial cells were unable to express MHC class II in response to IFN-gamma alone, these cells readily expressed MHC class II molecules via a CIITA-independent pathway when triggered by simultaneous exposure to IFN-gamma and TNF-alpha. CIITA-independent expression of MHCclass II molecules enabled corneal endothelial cells to present cytosolic, but not endosomal, ovalbumin (OVA) to OVA-primed T cells. To determine whether CIITA-independent expression of MHC class II is relevant in vivo, minor H-only-incompatible corneal allografts prepared from CIITA knockout (KO) mice, MHC class II KO mice or wild-type donors were placed in eyes of normal mice. Cornea allografts from wild-type and CIITA KO mice suffered similar rejection fates, whereas far fewer class II-deficient corneas were rejected. In addition, MHC class II-bearing macrophages were observed in cuprizone-induced inflammatory and demyelinating brain lesions of CIITA KO mice. We conclude that class II expression via the CIITA-independent pathway enhances the vulnerability to rejection of corneal grafts expressing minor antigens. The potential relevance of CIITA-independent MHC class II expression at immune-privileged sites is discussed in relation to tolerance to strong autoantigens. |
