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CD99 Regulates the Transport of MHC Class I Molecules from the Golgi Complex to the Cell Surface¹

Hae Won Sohn^*, Young Kee Shin, Im-Soon Lee, Young Mee Bae, Young Ho Suh^*, Min Kyung Kim^*, Tae Jin Kim^#, Kyeong Cheon Jung^*, Weon Seo Park, Chan-Sik Park^*, Doo Hyun Chung^*, Kwangseog Ahn^¶, In Sun Kim, Young Hyeh Ko^||, Yung Jue Bang, Chul Woo Kim^* and Seong Hoe Park^2,*,

Department of ^* Pathology and Internal Medicine, Seoul National University College of Medicine, Seoul, Korea; Institute of Allergy and Clinical Immunology, Seoul National University, Seoul, Korea; Department of Pathology, Korea University College of Medicine, Seoul, Korea; ^¶ Graduate School of Biotechnology, Korea University, Seoul, Korea; ^|| Department of Diagnostic Pathology, Samsung Medical Center, Seoul, Korea; ^# Department of Pathology, Sungkyunkwan University College of Medicine, Suwon, Korea; ^** DiNonA, Suwon, Korea; Department of Pathology, Kangwon National University College of Medicine, Chunchon, Korea; and ^* Department of Pathology, Hallym University College of Medicine, Chunchon, Korea

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 -mannosidase II and -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.

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