Transcriptional downregulation of DC-SIGN in human herpesvirus 6-infected dendritic cells.
DC-SIGN expressed on dendritic cells (DCs) efficiently binds and transmits various pathogens, including human immunodeficiency virus, to lymphoid tissues and permissive cells. Consequently, alteration of DC-SIGN expression may affect susceptibility and resistance to pathogens. The present study shows that infection with human herpesvirus 6 (HHV-6) induces downregulation of DC-SIGN expression on immature DCs. Expression levels of DC-SIGN mRNA and intracellular protein appeared to decrease following infection with HHV-6, indicating that downregulation of surface DC-SIGN occurs at the transcriptional level. Downregulation of DC-SIGN was not induced by inoculation of UV-inactivated HHV-6 or culture supernatant of HHV-6-infected DCs, indicating that replication of HHV-6 in DCs is required for downregulation of DC-SIGN. The present study demonstrates for the first time that expression of DC-SIGN is altered at the transcriptional level by virus infection.
Niiya
Hironari
H
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Azuma
Taichi
T
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Jin
Lei
L
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Uchida
Naoyuki
N
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Inoue
Atsushi
A
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Hasegawa
Hitoshi
H
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Fujita
Shigeru
S
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Tohyama
Mikiko
M
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Hashimoto
Koji
K
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
Yasukawa
Masaki
M
First Department of Internal Medicine and Department of Dermatology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan.
D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D003713:Dendritic Cells / Q000378:metabolism / Q000821:virology*; D015536:Down-Regulation; D015654:Herpesvirus 6, Human / Q000502:physiology* / Q000528:radiation effects; D006801:Humans; D037181:Lectins, C-Type / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D011991:Receptors, Virus / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic; D014466:Ultraviolet Rays; D014779:Virus Replication; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
D015815:Cell Adhesion Molecules; D037181:Lectins, C-Type; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D011991:Receptors, Virus; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin