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Blood, 1 May 2001, Vol. 97, No. 9, pp. 2764-2771
IMMUNOBIOLOGY
Stimulation of autologous proliferative and cytotoxic T-cell
responses by "leukemic dendritic cells" derived from blast cells in
acute myeloid leukemia
Beth D. Harrison,
Julie A. Adams,
Mark Briggs,
Michelle L. Brereton, and
John
A. Liu Yin
From the University Department of Haematology,
Manchester Royal Infirmary, Manchester, United Kingdom.
Effective presentation of tumor antigens is fundamental to
strategies aimed at enrolling the immune system in eradication of
residual disease after conventional treatments. Myeloid malignancies provide a unique opportunity to derive dendritic cells (DCs), functioning antigen-presenting cells, from the malignant cells themselves. These may then co-express leukemic antigens together with
appropriate secondary signals and be used to generate a specific, antileukemic immune response. In this study, blasts from 40 patients with acute myeloid leukemia (AML) were cultured with combinations of
granulocyte-macrophage colony-stimulating factor, interleukin 4, and
tumor necrosis factor  , and development to DCs was assessed. After
culture, cells from 24 samples exhibited morphological and immunophenotypic features of DCs, including expression of major histocompatibility complex class II, CD1a, CD83, and CD86, and were
potent stimulators in an allogeneic mixed lymphocyte reaction (MLR).
Stimulation of autologous T-cell responses was assessed by the
proliferative response of autologous T cells to the leukemic DCs and by
demonstration of the induction of specific, autologous, antileukemic
cytotoxicity. Of 17 samples, 11 were effective stimulators in
the autologous MLR, and low, but consistent, autologous, antileukemic cytotoxicity was induced in 8 of 11 cases (mean, 27%; range,
17%-37%). This study indicates that cells with enhanced
antigen-presenting ability can be generated from AML blasts, that these
cells can effectively prime autologous cytotoxic T cells in vitro, and
that they may be used as potential vaccines in the immunotherapy of AML.
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