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Published on: March 26, 2018
Expression of CD86 in acute myelogenous leukemia is a marker of dendritic/monocytic lineage
Francesca Re1, Mario Arpinati, Nicoletta Testoni
1Institute of Hematology and Medical Oncology Seràgnoli, University of Bologna, Bologna, Italy.
Insights
CD86 expression in acute myeloid leukemia (AML) identifies monocytic/dendritic lineage cells. These CD86(+) AML cells can rapidly differentiate into dendritic cells, making them promising candidates for immunotherapy.
Area of Science:
- Hematology
- Immunology
- Cancer Biology
Background:
- Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy.
- The monocytic/dendritic lineage commitment of AML blast cells remains incompletely understood.
- Identifying specific markers can aid in understanding AML differentiation pathways.
Purpose of the Study:
- To investigate the expression of the CD86 costimulatory molecule in AML.
- To determine if CD86 expression can identify AML blast cells committed to the monocytic/dendritic lineage.
- To explore the potential of CD86(+) AML cells for immunotherapy.
Main Methods:
- Flow cytometry analysis of 110 AML patients at diagnosis.
- In vitro differentiation of CD86(+) AML blasts into dendritic cells (DCs) using GM-CSF, TNF-alpha, and IL-4.
- Morphologic and immunophenotypic characterization of differentiated cells.
- Assessment of T-cell alloreactivity and anti-leukemic cytotoxicity against AML-derived DCs.
Main Results:
- CD86 was expressed in 54% of AML patients, often co-expressed with CD14 and inversely with CD34.
- CD86(+) AML cells, particularly CD34(+)CD86(+) and CD34(-)CD86(+) subsets, differentiated into leukemic dendritic cells (AML-DCs) expressing DC markers (CD80, CD40, CD11c, HLA-DR, CD1a/CD83).
- AML-DCs induced stronger allo-T-cell proliferation, cytokine release, and anti-leukemic cytotoxicity compared to CD86(+) blasts.
Conclusions:
- CD86 serves as a reliable marker for monocytic/dendritic lineage commitment in AML.
- The rapid differentiation potential of CD86(+) AML blasts into functional DCs suggests their utility in immunotherapy.
- CD86(+) AML patients represent potential candidates for autologous and allogeneic immunotherapy strategies.
Objective:
The aim of this study was to determine whether expression of the CD86 costimulatory molecule in acute myeloid leukemia (AML) can identify blast cells committed to the monocytic/dendritic lineage.
Material And Methods:
One hundred ten consecutive AML patients observed at diagnosis were studied by flow cytometry. In selected experiments, in vitro cultures with CD34(+)CD86(+) or CD34(-)CD86(+) blasts were performed in the presence of granulocyte-macrophage colony-stimulating actor (GM-CSF) with or without tumor necrosis factor-alpha (TNF-alpha) or GM-CSF + interleukin-4 (IL-4), respectively, to induce a dendritic differentiation, documented by morphologic and immunophenotypic assays. T-cell alloreactivity to CD86(+) AML cells and leukemic dendritic cells (AML-DC) was tested in mixed leukocyte cultures and anti-leukemic cytotoxic assays.
Results:
CD86 was expressed in 54% AML, whereas CD80 and CD1a were only occasionally positive. CD86(+) AML samples included M5 and M4, but also 47% M0-M1 FAB types, and were more frequently CD14(+) (p < 0.00001) and CD34(-) (p = 0.00005) than CD86(-)AML. Six different patterns of CD86(+) AML were identified, according to CD34 or CD14 total or partial coexpression. Four samples enriched in CD34(+)CD86(+) AML cells differentiated into AML-DC CD86(+), CD80(+), CD40(+), CD11c(+), HLA-DR(++), CD14(+/-) that also were CD1a(+) or CD83(+), after 6 days of in vitro culture with GM-CSF +/- TNF-alpha. CD34(-)CD86(+) AML cells differentiated into AML-DC after 3 to 5 days (n = 5 experiments), and trisomy 8 was found in two AML and AML-DC samples by fluorescence in situ hybridization analysis. Finally, AML-DC induced more potent allo-T-cell proliferation, cytokine release, and anti-leukemic cytotoxicity than CD86(+) blasts.
Conclusions:
In AML, CD86 is a marker of monocytic/dendritic lineage. Because CD86(+) blasts may differentiate into DC rapidly, CD86(+)AML patients could be optimal candidates for immunotherapy studies, both in autologous and allogeneic settings.
