Dendritic cell activation prevents MHC class II ubiquitination and promotes MHC class II survival regardless of the activation stimulus.
The expression of MHC class II (MHC-II) on the surface of antigen-presenting cells, such as dendritic cells (DCs), is tightly regulated during cellular activation. Many cells, including DCs, are activated following stimulation of innate Toll-like receptors (TLRs) by products of microorganisms. In the resting (immature) state, MHC-II is ubiquitinated in immature DCs and is rapidly degraded; however, after activation of these cells with MyD88-dependent TLR ligands, MHC-II ubiquitination is blocked, and MHC-II survival is prolonged. We now show that DC activation using MyD88-dependent TLR ligands, MyD88-independent TLR ligands, and even infection with the intracellular parasite Toxoplasma gondii leads to identical changes in MHC-II expression, ubiquitination, and surface stability, revealing a conserved role for enhanced MHC-II stability after DC activation by different stimuli.
Experimental Immunology Branch, NCI, National Institutes of Health, Frederick, Maryland 21702, USA.
Even
E
Walseng
Kazuyuki
K
Furuta
Romina S
RS
Goldszmid
Karis A
KA
Weih
Alan
A
Sher
Paul A
PA
Roche
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D002469:Cell Separation; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology*; D005434:Flow Cytometry; D000949:Histocompatibility Antigens Class II / Q000737:chemistry*; D006801:Humans; D008024:Ligands; D051379:Mice; D009000:Monocytes / Q000166:cytology; D013499:Surface Properties; D051193:Toll-Like Receptors / Q000378:metabolism; D014122:Toxoplasma / Q000378:metabolism; D015854:Up-Regulation
D000949:Histocompatibility Antigens Class II; D008024:Ligands; D051193:Toll-Like Receptors