ArticleFrontiers in immunology2022
Indoleamine 2, 3-Dioxygenase 1 Mediates Survival Signals in Chronic Lymphocytic Leukemia
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Aryl Hydrocarbon Receptor in Health and Disease.MedComm · 2025Review
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- The Aryl Hydrocarbon Receptor Regulates Invasiveness and Motility in Acute Myeloid Leukemia Cells through Expressional Regulation of Non-Muscle Myosin Heavy Chain IIA.International journal of molecular sciences · 2024Article
- Article
- The aryl hydrocarbon receptor as a tumor modulator: mechanisms to therapy.Frontiers in oncology · 2024Review
- The tryptophan-kynurenine pathway in immunomodulation and cancer metastasis.Cancer medicine · 2023Review
- Functions of the aryl hydrocarbon receptor (AHR) beyond the canonical AHR/ARNT signaling pathway.Biochemical pharmacology · 2023Review
- The signaling function of IDO1 incites the malignant progression of mouse B16 melanoma.Oncoimmunology · 2023Article
- Polyphenols: Chemoprevention and therapeutic potentials in hematological malignancies.Frontiers in nutrition · 2022Review
- Single-Cell Metabolomics in Hematopoiesis and Hematological Malignancies.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The indoleamine 2,3-dioxygenase 1 (IDO1) metabolic circuitry, comprising the first tryptophan (Trp) catabolite L-kynurenine (Kyn) and the aryl hydrocarbon receptor (AHR), has emerged as a mechanism of cancer immune evasion. Here, we investigated the functional role of the IDO1/Kyn/AHR axis in chronic lymphocytic leukemia (CLL). Our data show that CLL cells expressed an active form of the IDO1 enzyme and microenvironmental stimuli can positively modulate its expression. Interferon (IFN)-γ induces IDO1 expression through the Jak/STAT1 pathway and mediates Kyn production concomitantly with Trp consumption in CLL-conditioned media, while INCB018424 (ruxolitinib), a JAK1/2 inhibitor, impaired both effects. To characterize the involvement of IDO1 in leukemic cell maintenance, we overexpressed IDO1 by vector transfection measuring enhanced resistance to spontaneous apoptosis. IDO1 pro-survival influence was confirmed by treating CLL cells with Kyn, which mediated the increase of induced myeloid leukemia cell differentiation protein (MCL1). Conversely, AHR silencing or its blockade
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