| First Author | Fu H | Year | 2009 |
| Journal | Mol Immunol | Volume | 46 |
| Issue | 16 | Pages | 3198-206 |
| PubMed ID | 19748124 | Mgi Jnum | J:155236 |
| Mgi Id | MGI:4413382 | Doi | 10.1016/j.molimm.2009.08.012 |
| Citation | Fu H, et al. (2009) Calreticulin maintains the low threshold of peptide required for efficient antigen presentation. Mol Immunol 46(16):3198-206 |
| abstractText | Calreticulin (CRT) plays a critical role in MHC class I antigen processing and elicits peptide-specific CD8(+) T cell responses against tumours when administered with peptides. However, how CRT contributes to class I antigen processing and the mechanism of its adjuvant effect in anti-tumour responses, remain to be elucidated. Here we show that reduced class I expression in CRT deficient cells can be restored by the direct delivery of peptides into the ER or by incubation at low temperature. CRT deficient cells exhibited a TAP-deficient phenotype in terms of class I assembly, without loss of TAP expression or functionality. Furthermore, a higher concentration of antigen in the cytosol is required for specific T cell stimulation, suggesting that CRT has a functional role in the maintenance of the low peptide concentration threshold required in the ER for efficient antigen presentation. In the absence of CRT, ERp57 is up-regulated, which indicates that they collaborate with each other in class I antigen processing. |
