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 Blood, 1 April 2007, Vol. 109, No. 7, pp. 2985-2988.
Prepublished online as a Blood First Edition Paper on November 21, 2006; DOI 10.1182/blood-2006-07-032839.

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IMMUNOBIOLOGY

Brief Report

A neoepitope generated by an FLT3 internal tandem duplication (FLT3-ITD) is recognized by leukemia-reactive autologous CD8+ T cells

Claudine Graf, Florian Heidel, Stefan Tenzer, Markus P. Radsak, Fian K. Solem, Cedrik M. Britten, Christoph Huber, Thomas Fischer, and Thomas Wölfel

1 III Medizinische Klinik, Johannes Gutenberg-Universität, Mainz, Germany; 2 Institut für Immunologie, Johannes Gutenberg-Universität, Mainz, Germany

The FLT3 receptor tyrosine kinase is expressed in more than 90% of acute myelogeneous leukemias (AMLs), up to 30% of which carry an internal tandem duplication (ITD) within the FLT3 gene. Although varying duplication sites exist, most FLT3-ITDs affect a single protein domain. We analyzed the FLT3-ITD of an AML patient for encoding HLA class I–restricted immunogenic peptides. One of the tested peptides (YVDFREYEYY) induced in vitro autologous T-cell responses restricted by HLA-A*0101 that were also detectable ex vivo. These peptide-reactive T cells recognized targets transfected with the patient's FLT3-ITD, but not wild-type FLT3, and recognized the patient's AML cells. Our results demonstrate that AML leukemic blasts can in principle process and present immunogenic FLT3-ITD neoepitopes. Therefore, FLT3-ITD represents a potential candidate target antigen for the immunotherapy of AML.


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