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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1528-1536.
Prepublished online as a Blood First Edition Paper on October 20, 2005; DOI 10.1182/blood-2005-05-2073.
Previous Article | Next Article 
Submitted May 23, 2005
Accepted October 11, 2005
Engagement of CD83 ligand induces prolonged expansion of CD8+ T cells and preferential enrichment for antigen specificity
Naoto Hirano*, Marcus O Butler, Zhinan Xia, Sascha Ansen, Michael S von Bergwelt-Baildon, Donna Neuberg, Gordon J Freeman, and Lee M Nadler
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA
Department of Biostatics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA
* Corresponding author; email: Naoto_HIrano{at}dfci.harvard.edu.
Following T cell receptor and CD28 signaling, CD8+ T cells express a receptor for CD83, a molecule upregulated on functionally mature dendritic cells. Though this expression pattern suggests that CD83 is involved in adaptive immunity, little is known about its function in the periphery, and the existence of its ligand on T cells is controversial. We demonstrate that the engagement of the CD83 ligand preferentially enriches and significantly amplifies the number of antigen-specific CD8+ T cells. Coengagement of the T cell receptor, CD28, and CD83 ligand supports priming of naive CD8+ T cells that retain antigen specificity and cytotoxic function for greater than 6 months. Therefore, engagement of the CD83 ligand provides a unique signal to activated CD8+ T cells that could be exploited to generate long-lived antigen specific cytotoxic T cells for the treatment of cancer and infection.

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