| First Author | McGehee AM | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 4 | Pages | e18817 |
| PubMed ID | 21533087 | Mgi Jnum | J:238328 |
| Mgi Id | MGI:5819060 | Doi | 10.1371/journal.pone.0018817 |
| Citation | McGehee AM, et al. (2011) Ubiquitin-dependent control of class II MHC localization is dispensable for antigen presentation and antibody production. PLoS One 6(4):e18817 |
| abstractText | Controlled localization of class II MHC molecules is essential for proper class II MHC-restricted antigen presentation and the subsequent initiation of an adaptive immune response. Ubiquitination of class II MHC molecules on cytosolic lysine (K225) of the beta-chain has been shown to affect localization of the complex. We generated mice in which the endogenous beta-chain locus is replaced with a GFP tagged mutant version that lacks the cytosolic lysine residue (I-A-beta-K225R-EGFP). These mice have elevated levels of class II MHC as compared to I-A-beta-EGFP mice, and immature bone marrow-derived dendritic cells show redistribution of class II MHC to the cell surface. Nonetheless, in these same cells efficiency of antigen presentation is unaffected in I-A-beta-K225R-EGFP mice, as assayed for presentation of ovalbumin to appropriately specific T cells. The I-A-beta-K225R-EGFP animals have normal CD4 T cell populations and are capable of generating antigen-specific antibody in response to model antigens and viral infection. We therefore conclude that in our experimental system modulation of trafficking by ubiquitination of residue K225 of the beta-chain is not essential for the function of class II MHC products in antigen presentation or antibody production. |
