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This article is part of the supplement: 2005 International Meeting of The Institute of Human Virology

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Activation and Maturation of Human Dendritic Cells by Extracellular Tax Protein of HTLV-1

Pooja Jain1*, Jaya Ahuja1, Zafar K Khan2, Saori Shimizu3, Olimpia Meucci3 and Brian Wigdahl1

  • * Corresponding author: Pooja Jain

Author Affiliations

1 Department of Microbiology and Immunology, Drexel University, Philadelphia, PA, USA

2 Department of Bioscience and Biotechnology, Drexel University, Philadelphia, PA, USA

3 Department of Pharmacology and Physiology, and Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine

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Retrovirology 2005, 2(Suppl 1):P38  doi:10.1186/1742-4690-2-S1-P38

The electronic version of this article is the complete one and can be found online at:

Published:8 December 2005


Poster presentation

HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is characterized by the generation of an intense cytotoxic T cell (CTL) response directed against oncoprotein Tax. Previous studies have suggested that Tax may be available for immune recognition by dendritic cells (DCs). In this study, we have shown that purified Tax protein efficiently bound and localized to the cell membrane of monocyte-derived dendritic cells (MDDCs) and was internalized within a few hours. After uptake, Tax-induced expression of DC activation markers MHC class I and II, and costimulatory molecules as well as the DC maturation marker, CD83. Tax has also promoted the production of major immune-directing cytokines IL-12, TNF-α, and proinflammatory chemokines MIP-1α, MIP-1β, and RANTES. The inhibitors of NF-κB have abrogated Tax-induced secretion of cytokines/chemokines indicating a role for NF-κB signaling in Tax-mediated immune response. Finally, Tax enhanced the allogenic and antigen-specific T cell proliferation capability of MDDCs. These results have indicated that extracellular Tax may selectively target MDDCs, be taken up by these cells and promote their maturation and antigen-presenting functions, driving a Th1-type immune response.