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Journal of Virology, August 2003, p. 8719-8728, Vol. 77, No. 16
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.16.8719-8728.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Induction of Protective Immune Responses against R5 Human Immunodeficiency Virus Type 1 (HIV-1) Infection in hu-PBL-SCID Mice by Intrasplenic Immunization with HIV-1-Pulsed Dendritic Cells: Possible Involvement of a Novel Factor of Human CD4+ T-Cell Origin

Atsushi Yoshida,1 Reiko Tanaka,1 Tsutomu Murakami,1 Yoshiaki Takahashi,1 Yoshio Koyanagi,2 Masataka Nakamura,3 Mamoru Ito,4 Naoki Yamamoto,5 and Yuetsu Tanaka1*

Department of Immunology, Graduate School and Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa 903-0215,1 Department of Virology, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575,2 Department of Molecular Virology and,5 Human Gene Science Center, Tokyo Medical and Dental University, Chiyoda-ku, Tokyo 113-8519,3 Central Institute for Experimental Animals, Kawasaki, Kanagawa 216-0001, Japan4

Received 20 February 2003/ Accepted 20 May 2003

The potential of a dendritic cell (DC)-based vaccine against human immunodeficiency virus type 1 (HIV-1) infection in humans was explored with SCID mice reconstituted with human peripheral blood mononuclear cells (PBMC). HIV-1-negative normal human PBMC were transplanted directly into the spleens of SCID mice (hu-PBL-SCID-spl mice) together with autologous mature DCs pulsed with either inactivated HIV-1 (strain R5 or X4) or ovalbumin (OVA), followed by a booster injection 5 days later with autologous DCs pulsed with the same respective antigens. Five days later, these mice were challenged intraperitoneally with R5 HIV-1JR-CSF. Analysis of infection at 7 days postinfection showed that the DC-HIV-1-immunized hu-PBL-SCID-spl mice, irrespective of the HIV-1 isolate used for immunization, were protected against HIV-1 infection. In contrast, none of the DC-OVA-immunized mice were protected. Sera from the DC-HIV-1- but not the DC-OVA-immunized mice inhibited the in vitro infection of activated PBMC and macrophages with R5, but not X4, HIV-1. Upon restimulation with HIV-1 in vitro, the human CD4+ T cells derived from the DC-HIV-1-immunized mice produced a similar R5 HIV-1 suppressor factor. Neutralizing antibodies against human RANTES, MIP-1{alpha}, MIP-1ß, alpha interferon (IFN-{alpha}), IFN-ß, IFN-{gamma}, interleukin-4 (IL-4), IL-10, IL-13, IL-16, MCP-1, MCP-3, tumor necrosis factor alpha (TNF-{alpha}), or TNF-ß failed to reverse the HIV-1-suppressive activity. These results show that inactivated HIV-1-pulsed autologous DCs can stimulate splenic resident human CD4+ T cells in hu-PBL-SCID-spl mice to produce a yet-to-be-defined, novel soluble factor(s) with protective properties against R5 HIV-1 infection.

* Corresponding author. Mailing address: Department of Immunology, Faculty of Medicine, University of the Ryukyus, Uehara 207, Nishihara-cho, Okinawa 903-0215, Japan. Phone: 81-98-895-1202. Fax: 81-98-895-1437. E-mail: yuetsu{at}ma.kcom.ne.jp.

Journal of Virology, August 2003, p. 8719-8728, Vol. 77, No. 16
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.16.8719-8728.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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