“…Despite this unremarkable role for ubiquitination in regulating the cell biology of MHC-II expression, studies have attributed MHC-II turnover to a wide variety of immunological phenomena in MHC-II ubiquitination-deficient mice, including modulation of regulatory T cell generation (12,13), affinity maturation in germinal centers (9), DnaK-induced alloimmunity (31), MHC class I expression and function on DCs (32), and migration of CD206 + DCs to skin-draining lymph nodes (14). Incubation of MHC-II ubiquitination-deficient DCs with specific Ags ex vivo enhances expression of Ag-specific pMHC-II (2,12), a phenomenon that has been proposed to reflect enhanced Ag presentation by these cells in vivo (12).…”