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ido1 inhibitor  (MedChemExpress)


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    Structured Review

    MedChemExpress ido1 inhibitor
    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + <t>IDO1</t> + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
    Ido1 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 968 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ido1+inhibitor/pmc13042794-263-10-5?v=MedChemExpress
    Average 97 stars, based on 968 article reviews
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    Images

    1) Product Images from "Metabolic Alterations in Macrophage Subtypes Propel Immune and Stromal Remodeling in Neurofibroma's Malignant Progression"

    Article Title: Metabolic Alterations in Macrophage Subtypes Propel Immune and Stromal Remodeling in Neurofibroma's Malignant Progression

    Journal: MedComm

    doi: 10.1002/mco2.70709

    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + IDO1 + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
    Figure Legend Snippet: Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + IDO1 + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

    Techniques Used: Expressing, Microscopy, Cell Culture, Migration, Cytometry



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    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + <t>IDO1</t> + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + <t>IDO1</t> + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + <t>IDO1</t> + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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    Effects of IgE activation <t>and</t> <t>IDO1/TDO</t> inhibition on mast-cell tryptase expression and histamine release. A Immunofluorescence staining showing tryptase (TPS) expression in LAD2 mast cells before IgE activation and after IgE activation. Tryptase levels were markedly reduced in the activated state following treatment with the IDO1/TDO inhibitor <t>HY-149,411.</t> Scale bar = 50 μm. B ELISA quantification of histamine (HIS) release in IgE-activated LAD2 mast cells treated with HY-149,411 under different tryptophan concentrations (IgE + HS+HY, IgE + MHS+HY, IgE + BS+HY, IgE + RS+HY). * P < 0.05, ** P < 0.01
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    Effects of IgE activation <t>and</t> <t>IDO1/TDO</t> inhibition on mast-cell tryptase expression and histamine release. A Immunofluorescence staining showing tryptase (TPS) expression in LAD2 mast cells before IgE activation and after IgE activation. Tryptase levels were markedly reduced in the activated state following treatment with the IDO1/TDO inhibitor <t>HY-149,411.</t> Scale bar = 50 μm. B ELISA quantification of histamine (HIS) release in IgE-activated LAD2 mast cells treated with HY-149,411 under different tryptophan concentrations (IgE + HS+HY, IgE + MHS+HY, IgE + BS+HY, IgE + RS+HY). * P < 0.05, ** P < 0.01
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    <t>IDO1</t> expression was related to poor prognosis in HCC. ( A) Representative images of IDO1 immunofluorescence staining of HCC tissue and paracancerous tissue in patients with HCC and quantitative results of the fluorescence intensity of IDO1. ( B ) Kaplan–Meier curves for OS in HCC patients based on IDO1expression level. ( C ) The IDO1 expression grouped by age, gender ( D ), tumor size ( E ), stage ( F ), AFP ( G ), HBV ( H ), cirrhosis ( I ), metastasis ( J ), relapse ( K ) and HBcAb ( L ). The data were presented as mean ± SEM (* P < 0.05).
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    Image Search Results


    Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + IDO1 + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

    Journal: MedComm

    Article Title: Metabolic Alterations in Macrophage Subtypes Propel Immune and Stromal Remodeling in Neurofibroma's Malignant Progression

    doi: 10.1002/mco2.70709

    Figure Lengend Snippet: Metabolic alterations in SPP1 + KYNU + macrophages remodel the immunosuppressive microenvironment in MPNST. (A) Representative image of mIHC results displaying the expression differences of SPP1 + KYNU + /SPP1 + IDO1 + macrophages (SPP1 + KYNU + CD163 + /SPP1 + IDO1 + CD163 + ) in PNF and MPNST tissues, captured at 40× (scale bars: 100 µm) and 120× magnification (scale bars: 50 µm), with quantification of SPP1 + KYNU + and SPP1 + IDO1 + cells per HP ( n = 3); (B) Live‐cell microscopy of Schwann cell (ipNF05.5) dynamics co‐cultured with macrophages over 48 h, with quantitative analysis of migration speed using Livecyte kinetic cytometer. (C) Alterations in cytokine secretion levels by macrophages under NC‐OE, SPP1‐OE, and SPP1‐OE with IDO1 inhibitor treatment, with quantitative analysis ( n = 3). (D) Chord diagram showing key receptor–ligand interactions between different SPP1 + macrophage subpopulations and T cells. (E) Dot plot showing the differences in T cell expression of regulatory T cell (Treg) and exhausted T cell (Tex) markers between PNF and MPNST. (F) Representative image of mIHC results displaying the expression differences of PD‐1 + T cells (PD‐1 + CD8A + ) between benign and malignant neurofibromas, along with the spatial distribution of macrophages (CD68 + ). Quantitative data are presented as mean ± SD, with significance levels indicated as (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

    Article Snippet: Linrodostat (BMS‐986205, ONO‐7701), acquired from MedChemExpress, was used as the IDO1 inhibitor at a concentration of 1 μM in our study.

    Techniques: Expressing, Microscopy, Cell Culture, Migration, Cytometry

    Effects of IgE activation and IDO1/TDO inhibition on mast-cell tryptase expression and histamine release. A Immunofluorescence staining showing tryptase (TPS) expression in LAD2 mast cells before IgE activation and after IgE activation. Tryptase levels were markedly reduced in the activated state following treatment with the IDO1/TDO inhibitor HY-149,411. Scale bar = 50 μm. B ELISA quantification of histamine (HIS) release in IgE-activated LAD2 mast cells treated with HY-149,411 under different tryptophan concentrations (IgE + HS+HY, IgE + MHS+HY, IgE + BS+HY, IgE + RS+HY). * P < 0.05, ** P < 0.01

    Journal: Amino Acids

    Article Title: Tryptophan metabolism reprogramming regulates Th1/Th2 immune balance and inhibits mast cell activation

    doi: 10.1007/s00726-026-03508-2

    Figure Lengend Snippet: Effects of IgE activation and IDO1/TDO inhibition on mast-cell tryptase expression and histamine release. A Immunofluorescence staining showing tryptase (TPS) expression in LAD2 mast cells before IgE activation and after IgE activation. Tryptase levels were markedly reduced in the activated state following treatment with the IDO1/TDO inhibitor HY-149,411. Scale bar = 50 μm. B ELISA quantification of histamine (HIS) release in IgE-activated LAD2 mast cells treated with HY-149,411 under different tryptophan concentrations (IgE + HS+HY, IgE + MHS+HY, IgE + BS+HY, IgE + RS+HY). * P < 0.05, ** P < 0.01

    Article Snippet: For experiments involving metabolic inhibition, the dual IDO1/TDO inhibitor HY-149,411 (MedChemExpress) was added 30 min before anti-IgE stimulation and maintained throughout the incubation period.

    Techniques: Activation Assay, Inhibition, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay

    IDO1 expression was related to poor prognosis in HCC. ( A) Representative images of IDO1 immunofluorescence staining of HCC tissue and paracancerous tissue in patients with HCC and quantitative results of the fluorescence intensity of IDO1. ( B ) Kaplan–Meier curves for OS in HCC patients based on IDO1expression level. ( C ) The IDO1 expression grouped by age, gender ( D ), tumor size ( E ), stage ( F ), AFP ( G ), HBV ( H ), cirrhosis ( I ), metastasis ( J ), relapse ( K ) and HBcAb ( L ). The data were presented as mean ± SEM (* P < 0.05).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: IDO1 expression was related to poor prognosis in HCC. ( A) Representative images of IDO1 immunofluorescence staining of HCC tissue and paracancerous tissue in patients with HCC and quantitative results of the fluorescence intensity of IDO1. ( B ) Kaplan–Meier curves for OS in HCC patients based on IDO1expression level. ( C ) The IDO1 expression grouped by age, gender ( D ), tumor size ( E ), stage ( F ), AFP ( G ), HBV ( H ), cirrhosis ( I ), metastasis ( J ), relapse ( K ) and HBcAb ( L ). The data were presented as mean ± SEM (* P < 0.05).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Expressing, Immunofluorescence, Staining, Fluorescence

    The infiltration and prognostic significance of mature DCs subsets in HCC. ( A ) Representative images of immunofluorescence staining of CK, CD11C, MHCII, CD40, CD80, in cancer and paracancerous tissues from HCC patients. ( B ) Quantitative analysis of the percentage of CD11C + , CD11C + MHCII + , CD11C + CD80 + and CD11C + CD40 + DCs. ( C ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + DCs. ( D ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + MHCII + DCs. ( E ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + CD80 + DCs. ( F ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + CD40 + DCs. ( G ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + MHCII + DCs, according to Spearman correlation analysis. ( H ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + CD80 + DCs, according to Spearman correlation analysis. ( I ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + CD40 + DCs, according to Spearman correlation analysis. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: The infiltration and prognostic significance of mature DCs subsets in HCC. ( A ) Representative images of immunofluorescence staining of CK, CD11C, MHCII, CD40, CD80, in cancer and paracancerous tissues from HCC patients. ( B ) Quantitative analysis of the percentage of CD11C + , CD11C + MHCII + , CD11C + CD80 + and CD11C + CD40 + DCs. ( C ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + DCs. ( D ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + MHCII + DCs. ( E ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + CD80 + DCs. ( F ) Kaplan–Meier curves for OS in HCC patients based on the percentage of CD11C + CD40 + DCs. ( G ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + MHCII + DCs, according to Spearman correlation analysis. ( H ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + CD80 + DCs, according to Spearman correlation analysis. ( I ) The correlation between the percentage of IDO1 + staining area levels and the percentage of CD11C + CD40 + DCs, according to Spearman correlation analysis. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Immunofluorescence, Staining

    IDO1 inhibition could attenuate the EMT and malignant proliferation of SK-HEP1 in vitro. ( A ) Western blot analysis was used to detect the expression levels of Vimentin and IDO1 in control and experimental SK-HEP1 cells at 24 h after EPA intervention. GAPDH served as a loading control. The density of protein was measured using Quantity One software. ( B ) Western blot analysis was used to detect the expression levels of E-cadherin and PCNA in control and experimental SK-HEP1 cells at 24 h after EPA intervention. α-tubulin served as a loading control. The density of protein was measured using Quantity One software. ( C ) Relative mRNA levels of IDO1, E-cadherin, Vimentin, and PCNA were measured in SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01, *** P < 0.001).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: IDO1 inhibition could attenuate the EMT and malignant proliferation of SK-HEP1 in vitro. ( A ) Western blot analysis was used to detect the expression levels of Vimentin and IDO1 in control and experimental SK-HEP1 cells at 24 h after EPA intervention. GAPDH served as a loading control. The density of protein was measured using Quantity One software. ( B ) Western blot analysis was used to detect the expression levels of E-cadherin and PCNA in control and experimental SK-HEP1 cells at 24 h after EPA intervention. α-tubulin served as a loading control. The density of protein was measured using Quantity One software. ( C ) Relative mRNA levels of IDO1, E-cadherin, Vimentin, and PCNA were measured in SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01, *** P < 0.001).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Inhibition, In Vitro, Western Blot, Expressing, Control, Software

    IDO1 inhibition could improve the malignant biological behavior of SK-HEP1 cells in vitro. ( A ) The proliferation of SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h was evaluated using the Key Fluor 488 Click-iT Edu assay. ( B ) The proliferation rate of SK-HEP1cells in ( A ) was quantified in a bar graph. ( C ) The cell viability of SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h was assessed using the CCK-8 assay. The cell viability reported as fold change of EPA-treated vs control cells. ( D ) Representative images from the transwell assay (left) and migrating cells number analysis (right). ( E ) Representative images from the wound healing assay. The data were presented as mean ± SEM (* P < 0.05, *** P < 0.001).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: IDO1 inhibition could improve the malignant biological behavior of SK-HEP1 cells in vitro. ( A ) The proliferation of SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h was evaluated using the Key Fluor 488 Click-iT Edu assay. ( B ) The proliferation rate of SK-HEP1cells in ( A ) was quantified in a bar graph. ( C ) The cell viability of SK-HEP1 cells treated with 0, 2.5, 5, 10, and 20 μM EPA for 24 h was assessed using the CCK-8 assay. The cell viability reported as fold change of EPA-treated vs control cells. ( D ) Representative images from the transwell assay (left) and migrating cells number analysis (right). ( E ) Representative images from the wound healing assay. The data were presented as mean ± SEM (* P < 0.05, *** P < 0.001).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Inhibition, In Vitro, EdU Assay, CCK-8 Assay, Control, Transwell Assay, Wound Healing Assay

    IDO1 inhibition could delay the subcutaneous tumor formation of SK-HEP-1 cells in vivo. ( A ) Schematic protocol for animal experiment. ( B ) The tumor growth curve of mice and the representative diagrams of tumors in each group. ( C ) Tumor weight of the mice in control and EPA-treated group. ( D ) Immunofluorescence staining of IDO1 in tumor tissues in control and EPA-treated group. ( E ) The serum levels of Trp and Kyn were determined in mice from both the control and EPA-treated groups. ( F ) HE staining of tumor tissues in control and EPA-treated group. ( G ) Immunohistochemistry staining of PCNA in control and EPA-treated group. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01, *** P < 0.001).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: IDO1 inhibition could delay the subcutaneous tumor formation of SK-HEP-1 cells in vivo. ( A ) Schematic protocol for animal experiment. ( B ) The tumor growth curve of mice and the representative diagrams of tumors in each group. ( C ) Tumor weight of the mice in control and EPA-treated group. ( D ) Immunofluorescence staining of IDO1 in tumor tissues in control and EPA-treated group. ( E ) The serum levels of Trp and Kyn were determined in mice from both the control and EPA-treated groups. ( F ) HE staining of tumor tissues in control and EPA-treated group. ( G ) Immunohistochemistry staining of PCNA in control and EPA-treated group. The data were presented as mean ± SEM (* P < 0.05, ** P <0.01, *** P < 0.001).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Inhibition, In Vivo, Control, Immunofluorescence, Staining, Immunohistochemistry

    IDO1 inhibition could enhance immune cells response to tumor cells in vivo. ( A ) Immunofluorescence staining of CD11C, MHCII,CD80 and CD40 in tumor tissues in control and EPA-treated group. ( B ) Immunofluorescence staining of CD4 and CD8 in tumor tissues in control and EPA-treated group. The data were presented as mean ± SEM (* P < 0.05, *** P < 0.001).

    Journal: Journal of Hepatocellular Carcinoma

    Article Title: Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma

    doi: 10.2147/JHC.S530997

    Figure Lengend Snippet: IDO1 inhibition could enhance immune cells response to tumor cells in vivo. ( A ) Immunofluorescence staining of CD11C, MHCII,CD80 and CD40 in tumor tissues in control and EPA-treated group. ( B ) Immunofluorescence staining of CD4 and CD8 in tumor tissues in control and EPA-treated group. The data were presented as mean ± SEM (* P < 0.05, *** P < 0.001).

    Article Snippet: IDO1 catalytic inhibitor epacadostat (EPA) was purchased from MedChemExpress LLC (Shanghai, China).

    Techniques: Inhibition, In Vivo, Immunofluorescence, Staining, Control