| First Author | Grandea AG 3rd | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 2 | Pages | 213-22 |
| PubMed ID | 10981964 | Mgi Jnum | J:64177 |
| Mgi Id | MGI:1888829 | Doi | 10.1016/s1074-7613(00)00021-2 |
| Citation | Grandea AG 3rd, et al. (2000) Impaired assembly yet normal trafficking of MHC class I molecules in Tapasin mutant mice. Immunity 13(2):213-22 |
| abstractText | Loading of peptides onto major histocompatibility complex class I molecules involves a multifactorial complex that includes tapasin (TPN), a membrane protein that tethers empty class I glycoproteins to the transporter associated with antigen processing. To evaluate the in vivo role of TPN, we have generated Tpn mutant mice. In these animals, most class I molecules exit the endoplasmic reticulum (ER) in the absence of stably bound peptides. Consequently, mutant animals have defects in class I cell surface expression, antigen presentation, CD8+ T cell development, and immune responses. These findings reveal a critical role of TPN for ER retention of empty class I molecules. Tpn mutant animals should prove useful for studies on alternative antigen-processing pathways that involve post-ER peptide loading. |
