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  • Oral presentation
  • Open Access

Neutralizing antibodies against human T cell leukemia virus type-I (HTLV-1) eradicate HTLV-1 in combination with autologous peripheral blood mononuclear cells via antibody-dependent cellular cytotoxicity while preventing new infection

  • 1Email author,
  • 1,
  • 1,
  • 1 and
  • 2
Retrovirology201411 (Suppl 1) :O39

https://doi.org/10.1186/1742-4690-11-S1-O39

  • Published:

Keywords

  • Neutralize Antibody
  • Neutralize Antibody Response
  • 51Cr Release Assay
  • Envelope Gp46
  • Autologous Peripheral Blood Mononuclear Cell

In order to establish a basis for vaccine development against human T cell leukemia virus type-I (HTLV-1), we have evaluated the roles of anti-HTLV-1 neutralizing antibodies using a rat monoclonal antibody (mAb) against HTLV-1 envelope gp46 (LAT-27) and human polyclonal IgG purified from sera of HTLV-1-associated myelopathy (HAM) patients (HAM-IgG). LAT-27 and HAM-IgG completely blocked the HTLV-1-mediated syncytium formation and T-cell transformation in vitro. Interestingly, when these antibodies were added to the cultures of CD8+ T cell-depleted peripheral blood mononuclear cells (PBMCs) from HAM patients, proliferation of Tax-expressing T cells and HTLV-1 p24 production were blocked. In addition, co-culture of HTLV-1-immortalized T cells with autologous PBMCs in the presence of LAT-27 or HAM-IgG, but not F(ab)’2 fragment of LAT-27 or the other non-neutralizing anti-gp46 mAbs, resulted in eradication of Tax-expressing cells and the p24 production. A 51Cr release assay for 24 hours showed a significant killing of HTLV-1-infected T cells by autologous PBMCs in the presence of LAT-27 or HAM-IgG, but not F(ab)’2 fragment of LAT-27, in which depletion of CD16+ cells from the effector PBMCs significantly reduced the killing activity. Altogether, the present data demonstrated for the first time that anti-HTLV-1 gp46 neutralizing antibodies are capable of not only preventing new infection but also eliminating HTLV-1-infected cells in the presence of autologous PBMCs mainly via an antibody-dependent cellular cytotoxicity (ADCC) in vitro. Thus, a vaccine candidate that can elicit or boost anti-gp46 neutralizing antibody response may have a potential for prevention and therapy against HTLV-1 infection.

Authors’ Affiliations

(1)
Department of Immunology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan
(2)
Department of Microbiology, Kawasaki Medical School, Kurashiki, Okayama, Japan

Copyright

© Tanaka et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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