| First Author | Wilson KR | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 7 | Pages | e0200540 |
| PubMed ID | 30001419 | Mgi Jnum | J:264103 |
| Mgi Id | MGI:6192195 | Doi | 10.1371/journal.pone.0200540 |
| Citation | Wilson KR, et al. (2018) MARCH1-mediated ubiquitination of MHC II impacts the MHC I antigen presentation pathway. PLoS One 13(7):e0200540 |
| abstractText | Major histocompatibility complex class II (MHC II) expression and turn-over are regulated via its ubiquitination by the membrane associated RING-CH 1 (MARCH1) E3 ligase. Unexpectedly, we show that MHC II ubiquitination also impacts MHC I. Lack of MARCH1 in B cells and dendritic cells (DCs) resulted in a significant reduction in surface MHC I expression. This decrease was not directly caused by changes in MARCH1 ubiquitination of MHC I but indirectly by altered MHC II trafficking in the absence of its ubiquitination. Deletion of MHC II in March1-/- cells restored normal MHC I surface expression and replacement of wild type MHC II by a variant that could not be ubiquitinated caused a reduction in MHC I expression. Furthermore, these cells displayed inefficient presentation of peptide and protein antigen via MHC I to CD8+ T cells. In summary, we describe an unexpected intersection between MHC I and MHC II such that the surface expression of both molecules are indirectly and directly regulated by MARCH1 ubiquitination, respectively. |
