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Role of Follicular Dendritic Cells in the Early HIV‐1 Infection: In vitro Model without Specific Antibody
Author(s) -
Taruishi Midori,
Terashima Kazuo,
Dewan Md. Zahidunnabi,
Yamamoto Norio,
Ikeda Satoshi,
Kobayashi Daisuke,
Eishi Yoshinobu,
Yamazaki Momoko,
Furusaka Tohru,
Sugimoto Masahiro,
Ishii Masanori,
Kitamura Ken,
Yamamoto Naoki
Publication year - 2004
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2004.tb03480.x
Subject(s) - follicular dendritic cells , biology , antibody , in vitro , virology , microbiology and biotechnology , viral replication , immunology , virus , antigen presenting cell , cytotoxic t cell , genetics
About 90% of HIV‐1 RNA in the lymph nodes is reported to localize in follicular dendritic cells‐network (FDC‐NW) as early as several days after infection and as much as that in the late stage. But the mechanism remains to be fully understood. To elucidate the role of follicular dendritic cells (FDC) in the early stage of HIV‐1 infection, FDC‐like cell strains (FDCLC) were established and they were characterized in the co‐culture system with T cells for their effect on HIV‐1 trapping and replication in p24 immunoassay, immunohistochemistry as well as confocal and electronmicroscopy. Established FDCLC were positive for CNA‐42, S‐100α and intercellular desmosome‐like junctions. L‐SIGN and DC‐SIGN were also detected in FDCLC. Alu‐HIV‐1 PCR analysis showed no HIV‐1 integration in FDCLC. FDCLC trapped HIV‐1 and transferred them to uninfected MOLT‐4 T cells (MOLT‐4) efficiently in the absence of specific antibody. FDCLC also accelerated HIV‐1 replication in HIV‐1‐pre‐exposed MOLT‐4. These unique FDCLC effects were explained, at least partly, by the fact that FDCLC up‐regulated CD4 expression in MOLT‐4 and helped T cells escape from apoptosis in the co‐culture. These data suggest that FDC/FDCLC engage not only in trapping but also in active expansion of HIV‐1 in the absence of specific antibody.