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Updated: Sep 22, 2025
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New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
Published on: May 30, 2013
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Hostile Takeover: Tregs Expand in IFNγ-Rich AML Microenvironment
P Brent Ferrell1, Shahram Kordasti2
1Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee.
Summary
Higher interferon-gamma (IFNγ) in acute myeloid leukemia (AML) patients upregulates immunosuppressive genes in mesenchymal stem cells (MSCs). This interaction, driven by IDO1, expands regulatory T cells (Tregs) in AML.
Area of Science:
- Immunology
- Oncology
- Stem Cell Biology
Background:
- A subset of acute myeloid leukemia (AML) patients exhibit elevated interferon-gamma (IFNγ) levels.
- This elevated IFNγ influences the tumor microenvironment by interacting with mesenchymal stem cells (MSCs).
Discussion:
- IFNγ from leukemia cells upregulates immunosuppressive genes in MSCs, notably through indoleamine 2,3-dioxygenase 1 (IDO1) overexpression.
- This upregulation of IDO1 by MSCs, in turn, promotes the expansion of regulatory T cells (Tregs).
- The induction of Tregs requires the combined presence and interaction of both leukemia cells and MSCs, as IFNγ-high leukemia cells alone cannot induce Tregs.
Key Insights:
- A positive correlation exists between IDO1 and IFNG gene expression in the context of AML and MSCs.
- Mesenchymal stem cells play a crucial role in mediating the immunosuppressive effects of IFNγ in AML.
- The study highlights a novel mechanism for Treg expansion in AML driven by leukemia-MSC crosstalk.
Outlook:
- Further investigation into targeting the IDO1 pathway in MSCs could offer new therapeutic strategies for AML.
- Understanding this leukemia-MSC-Treg axis may lead to improved immunotherapies for AML patients.
- Exploring the role of other cytokines in modulating MSC function in AML is warranted.
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