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 Blood, 15 August 2008, Vol. 112, No. 4, pp. 1231-1239.
Prepublished online as a Blood First Edition Paper on June 2, 2008; DOI 10.1182/blood-2008-03-148072.

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Submitted March 31, 2008
Accepted May 3, 2008

Targeting the nuclear antigen 1 of Epstein Barr virus to the human endocytic receptor DEC-205 stimulates protective T-cell responses

Cagan Gurer, Till Strowig, Fabienne Brilot, Maggi Pack, Christine Trumpfheller, Frida Arrey, Chae Gyu Park, Ralph M Steinman, and Christian Munz*

Laboratory of Viral Immunobiology, The Rockefeller University, New York, New York, United States
Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, New York, United States
Christopher H. Brown Center for Immunology and Immune Diseases, The Rockefeller University, New York, New York, United States

* Corresponding author; email: munzc{at}rockefeller.edu.

Dendritic cells (DCs) express many endocytic receptors that deliver antigens for MHC class I and II presentation to CD8+ and CD4+ T cells, respectively. Here, we show that targeting Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) to one of them, the human multilectin DEC-205 receptor, in the presence of the DC maturation stimulus poly(I:C), expanded EBNA1 specific CD4+ and CD8+ memory T cells, and these lymphocytes could control the outgrowth of autologous EBV infected B cells in vitro. In addition, using a novel mouse model with reconstituted human immune system components, we demonstrated that vaccination with {alpha}DEC-205-EBNA1 antibodies primed EBNA1 specific IFN-{gamma} secreting T cells and also induced anti-EBNA1 antibodies in a subset of immunized mice. Since EBNA1 is the one EBV antigen that is expressed in all proliferating cells infected with this virus, our data suggest that DEC-205 targeting should be explored as a vaccination approach against symptomatic primary EBV infection and against EBV associated malignancies.


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