| First Author | Wu SJ | Year | 2017 |
| Journal | Cell Rep | Volume | 19 |
| Issue | 13 | Pages | 2645-2656 |
| PubMed ID | 28658614 | Mgi Jnum | J:255769 |
| Mgi Id | MGI:6114617 | Doi | 10.1016/j.celrep.2017.06.013 |
| Citation | Wu SJ, et al. (2017) A Critical Analysis of the Role of SNARE Protein SEC22B in Antigen Cross-Presentation. Cell Rep 19(13):2645-2656 |
| abstractText | Cross-presentation initiates immune responses against tumors and viral infections by presenting extracellular antigen on MHC I to activate CD8(+) T cell-mediated cytotoxicity. In vitro studies in dendritic cells (DCs) established SNARE protein SEC22B as a specific regulator of cross-presentation. However, the in vivo contribution of SEC22B to cross-presentation has not been tested. To address this, we generated DC-specific Sec22b knockout (CD11c-Cre Sec22b(fl/fl)) mice. Contrary to the paradigm, SEC22B-deficient DCs efficiently cross-present both in vivo and in vitro. Although in vitro small hairpin RNA (shRNA)-mediated Sec22b silencing in bone-marrow-derived dendritic cells (BMDCs) reduced cross-presentation, treatment of SEC22B-deficient BMDCs with the same shRNA produced a similar defect, suggesting the Sec22b shRNA modulates cross-presentation through off-target effects. RNA sequencing of Sec22b shRNA-treated SEC22B-deficient BMDCs demonstrated several changes in the transcriptome. Our data demonstrate that contrary to the accepted model, SEC22B is not necessary for cross-presentation, cautioning against extrapolating phenotypes from knockdown studies alone. |
