Abstract
Minimally differentiated acute myeloid leukemia (AML-M0) is a rare FAB subtype (2–3% of AMLs) of poor prognosis. The aim of our study was to characterize AML-M0 expression and regulation of adhesion/costimulatory molecule involved in immune recognition, to test blast in vitro immunogenicity, and to determine the percentage of leukemia progenitor cells. Here, we demonstrate that alloimmune recognition of AML-M0 in primary mixed lymphocyte reaction, as evaluated by IL-2 secretion of responding T cells, is reduced in comparison with more differentiated subtypes (128 ± 95 pg/ml vs304 ± 159 pg/ml, P < 0.05). these data are in line with low blast cell expression of major histocompatibility complex (mhc) class ii dr molecules, and of the cd28 ligand b7-2, which plays an important role in aml immune recognition. adhesion/costimulatory molecules were up-regulated by leukemic cell stimulation via cd40, and, although less efficiently, by γ-ifn; both stimuli improved blast cell immunogenicity. we also demonstrate that aml-m0 have a very high percentage (40% ± 30) of cd34+/CD38− leukemic clonogenic precursors in comparison with more differentiated AMLs (2.5% ± 2) or non-leukemic CD34+hematopoietic precursors (1.8% ± 0.8). Since the presence of a leukemic cell population at an early differentiation stage has been identified as a poor prognostic factor, we conclude that the high frequency of CD34+/CD38− blasts in AML-M0 may converge with already identified poor prognosis factors such as chemotherapy resistance and cytogenetic abnormalities. The clinical implications of AML-M0 impaired in vitroimmunogenicity and a high percentage of CD34+/CD38− blasts will require comparative analysis of additional patients. The increased immunogenicity of blast cells after CD40 triggering provide interesting clues for AML-M0 immunotherapy, that have to be confirmed with an in vivo leukemia model in mice.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 12 print issues and online access
$259.00 per year
only $21.58 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Costello, R., Mallet, F., Chambost, H. et al. The immunophenotype of minimally differentiated acute myeloid leukemia (AML-M0): reduced immunogenicity and high frequency of CD34+/CD38− leukemic progenitors. Leukemia 13, 1513–1518 (1999). https://doi.org/10.1038/sj.leu.2401519
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1038/sj.leu.2401519
Keywords
This article is cited by
-
Aberrant marker expression patterns on the CD34+CD38− stem cell compartment in acute myeloid leukemia allows to distinguish the malignant from the normal stem cell compartment both at diagnosis and in remission
Leukemia (2007)
-
Apoptosis induction in peripheral leukemia cells by remission induction treatment in vivo: selective depletion and apoptosis in a CD34+ subpopulation of leukemia cells
Leukemia (2003)
-
Characteristics and analysis of normal and leukemic stem cells: current concepts and future directions
Leukemia (2000)
-
Acute myeloid leukaemia triggering via CD40 induces leukocyte chemoattraction and cytotoxicity against allogenic or autologous leukemic targets
Leukemia (2000)