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International Immunology Advance Access originally published online on August 9, 2004
International Immunology 2004 16(10):1377-1389; doi:10.1093/intimm/dxh139
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© 2004 The Japanese Society for Immunology

Characterization of dendritic-like cells derived from t(9;22) acute lymphoblastic leukemia blasts

Jaewoo Lee1, Sheila N. Sait2 and Meir Wetzler1,3

1 Department of Immunology, 2 Clinical Cytogenetics Laboratory and 3 Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA

Correspondence to: M. Wetzler; E-mail: meir.wetzler{at}roswellpark.org

We asked herein whether functional dendritic-like cells could be generated from t(9;22) acute lymphoblastic leukemia (ALL) blasts. We first determined that the combination of interleukin (IL)-1ß, IL-3, IL-7, tumor necrosis factor-{alpha}, stem cell factor and CD40 ligand was optimal for generating dendritic-like cells from t(9;22) ALL cell lines. Following 6 days in culture, four of five cell lines demonstrated dendrite-like morphology, upregulation of CCR7, CD54, CD80 and CD86, uptake of extracellular proteins and activation of T cells, and similar results were obtained with blasts from three t(9;22) ALL patients. The dendritic-like cells appeared to be composed of populations resembling both immature and mature dendritic cells (DCs), distinguished by CD80 expression. CD80–CD86+ cells were classified as immature DCs, demonstrating high endocytic capability and inducing minimal allogeneic T cell proliferation, while CD80+CD86+ cells were classified as mature DCs, exhibiting negligible endocytic capability and inducing robust allogeneic T cell proliferation. These mature dendritic-like cells induced autologous cytotoxic T cell responses against the unmodified blasts in a patient who achieved prolonged remission. In summary, CD80+CD86+ cells generated from t(9;22) ALL blasts may be useful in adoptive immunotherapy for t(9;22) ALL.

Keywords: dendritic-like cell, acute lymphoblastic leukemia, maturation, t(9;22), Philadelphia chromosome

Transmitting editor: P. W. Kincade


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