ArticleCancer immunology, immunotherapy : CII2010
In acute myeloid leukemia, B7-H1 (PD-L1) protection of blasts from cytotoxic T cells is induced by TLR ligands and interferon-gamma and can be reversed using MEK inhibitors.
Article in Cancer immunology, immunotherapy : CII, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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89 citing papers in PubMed, 161 citations in OpenAlex.
- Phase II Trial of Pembrolizumab after High-Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia.Blood cancer discovery · 2021Trial
- TLR4 activation enhances the PD-L1-mediated tolerogenic capacity of colonic CD90+ stromal cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- 16S rRNA gene sequencing reveals distinct intratumoral bacterial microbiome signatures between CT indeterminate benign and early-stage malignant pulmonary lesions.Journal of translational medicine · 2026Article
- Pre-therapeutic bone marrow-resident leukemic cells in acute myeloid leukemia exhibit a distinct dysregulated calcium signature and stem-like profile reflecting minimal residual disease precursors.Journal of experimental & clinical cancer research : CR · 2026Article
- The tumor microenvironment in leukemia: molecular pathways of immune evasion.Frontiers in immunology · 2026Review
- PD-L1 Expression in Acute Myeloid Leukemia Cells: Associations With Cell Metabolism.Journal of immunology research · 2026Article
- Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.Nature cancer · 2025Article
- Review
- miR-128-3p Reduces Proliferation and Immune Escape in Acute Myeloid Leukemia Through Targeted Regulation of ZEB1.Applied biochemistry and biotechnology · 2025Article
- Review
- Monocytic Differentiation in Acute Myeloid Leukemia Cells: Diagnostic Criteria, Biological Heterogeneity, Mitochondrial Metabolism, Resistance to and Induction by Targeted Therapies.International journal of molecular sciences · 2024Review
- LILRB3 Modulates Acute Myeloid Leukemia Progression and Acts as an Effective Target for CAR T-cell Therapy.Cancer research · 2023Article
- Emerging and Future Targeted Therapies for Pediatric Acute Myeloid Leukemia: Targeting the Leukemia Stem Cells.Biomedicines · 2023Review
- Checkpoint Inhibitors in Acute Myeloid Leukemia.Biomedicines · 2023Review
- Review
- NK cell defects: implication in acute myeloid leukemia.Frontiers in immunology · 2023Review
- Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- A perspective of immunotherapy for acute myeloid leukemia: Current advances and challenges.Frontiers in pharmacology · 2023Review
- Programmed Cell Death Ligand 1 Expression Level and Prognostic Significance in Acute Myeloid Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022Article
- Targeting PD-1/PD-L1 pathway in myelodysplastic syndromes and acute myeloid leukemia.Experimental hematology & oncology · 2022Review
29 more citing papers are in PubMed but not listed here.
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8 authors at 3 institutions in 1 country.
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Abstract
B7-H1 (PD-L1) is a B7-related protein that inhibits T-cell responses. B7-H1 participates in the immunoescape of cancer cells and is also involved in the long-term persistence of leukemic cells in a mouse model of leukemia. B7-H1 can be constitutively expressed by cancer cells, but is also induced by various stimuli. Therefore, we examined the constitutive and inducible expression of B7-H1 and the consequences of this expression in human acute myeloid leukemia (AML). We analyzed B7-H1 expression in a cohort of 79 patients with AML. In addition, we studied blast cells after incubation with interferon-gamma or toll-like receptors (TLR) ligands. Finally, we evaluated functionality of cytotoxic T-cell activity against blast cells. Expression of B7-H1 upon diagnosis was high in 18% of patients. Expression of TLR2, 4 and 9 was detected in one-third of AML samples. Expression of TLR2 and TLR4 ligands or IFN-γ induced by B7-H1 was found to protect AML cells from CTL-mediated lysis. Spontaneous B7-H1 expression was also found to be enhanced upon relapse in some patients. MEK inhibitors, including UO126 and AZD6244, reduced B7-H1 expression and restored CTL-mediated lysis of blast cells. In AML, B7-H1 expression by blasts represents a possible immune escape mechanism. The inducibility of B7-H1 expression by IFN-γ or TLR ligands suggests that various stimuli, either produced during the immune response against leukemia cells or released by infectious microorganisms, could protect leukemic cells from T cells. The efficacy of MEK inhibitors against B7-H1-mediated inhibition of CTLs suggests a possible cancer immunotherapy strategy using targeted drugs.
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