title: CD99 regulates the transport of MHC class I molecules from the Golgi complex to the cell surface.
abstract: The down-regulation of surface expression of MHC class I molecules has recently been reported in the CD99-deficient lymphoblastoid B cell line displaying the characteristics of Hodgkin's and Reed-Sternberg phenotype. Here, we demonstrate that the reduction of MHC class I molecules on the cell surface is primarily due to a defect in the transport from the Golgi complex to the plasma membrane. Loss of CD99 did not affect the steady-state expression levels of mRNA and protein of MHC class I molecules. In addition, the assembly of MHC class I molecules and the transport from the endoplasmic reticulum to the cis-Golgi occurred normally in the CD99-deficient cells, and no difference was detected between the CD99-deficient and the control cells in the pattern and degree of endocytosis. Instead, the CD99-deficient cells displayed the delayed transport of newly synthesized MHC class I molecules to the plasma membrane, thus causing accumulation of the molecules within the cells. The accumulated MHC class I molecules in the CD99-deficient cells were colocalized with alpha-mannosidase II and gamma-adaptin in the Golgi compartment. These results suggest that CD99 may be associated with the post-Golgi trafficking machinery by regulating the transport to the plasma membrane rather than the endocytosis of surface MHC class I molecules, providing a novel mechanism of MHC class I down-regulation for immune escape.
authors.affiliation: Department of. Pathology and Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
authors.forename: H W
authors.initials: HW
authors.lastname: Sohn
authors.forename: Y K
authors.initials: YK
authors.lastname: Shin
authors.forename: I S
authors.initials: IS
authors.lastname: Lee
authors.forename: Y M
authors.initials: YM
authors.lastname: Bae
authors.forename: Y H
authors.initials: YH
authors.lastname: Suh
authors.forename: M K
authors.initials: MK
authors.lastname: Kim
authors.forename: T J
authors.initials: TJ
authors.lastname: Kim
authors.forename: K C
authors.initials: KC
authors.lastname: Jung
authors.forename: W S
authors.initials: WS
authors.lastname: Park
authors.forename: C S
authors.initials: CS
authors.lastname: Park
authors.forename: D H
authors.initials: DH
authors.lastname: Chung
authors.forename: K
authors.initials: K
authors.lastname: Ahn
authors.forename: I S
authors.initials: IS
authors.lastname: Kim
authors.forename: Y H
authors.initials: YH
authors.lastname: Ko
authors.forename: Y J
authors.initials: YJ
authors.lastname: Bang
authors.forename: C W
authors.initials: CW
authors.lastname: Kim
authors.forename: S H
authors.initials: SH
authors.lastname: Park
mesh_terms: D000071443:12E7 Antigen; D015703:Antigens, CD / Q000235:genetics / Q000502:physiology*; D001693:Biological Transport, Active / Q000235:genetics / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D002461:Cell Line, Transformed; D002462:Cell Membrane / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D015536:Down-Regulation / Q000235:genetics / Q000276:immunology; D004705:Endocytosis / Q000235:genetics / Q000276:immunology; D004721:Endoplasmic Reticulum / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D006056:Golgi Apparatus / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis / Q000378:metabolism*; D006801:Humans; D007700:Kinetics; D011499:Protein Processing, Post-Translational / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D000071443:12E7 Antigen; D015703:Antigens, CD; C061828:CD99 protein, human; D015815:Cell Adhesion Molecules; D015395:Histocompatibility Antigens Class I; D012333:RNA, Messenger