Journal: Inflammation Research

Article Title: IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression

doi: 10.1007/s00011-026-02223-8

Figure Lengend Snippet: The frequency of ILC1 is decreased, whereas ILC3 is increased, in IDH1-mutant human glioma tissues compared with the IDH1-wild-type group. A Representative flow-cytometry gating strategies for ILCs in human tonsil (control) tissue, IDH1-wildtype, and IDH1-mutant glioma tissue (FSC-A = forward-scatter area; SSC-A = side-scatter area). B Comparison of total ILC percentages in tonsil controls (n = 11), IDH1-wild-type (n = 9), and IDH1-mutant (n = 3) glioma tissues (top center); comparison of ILC1 percentages (bottom left), ILC2 percentages (bottom center), and ILC3 percentages (bottom right) across the same groups. C Comparison of mean fluorescence intensity (MFI) of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) expression on ILC1s in tonsil control, IDH1-wild-type, and IDH1-mutant groups. D Comparison of MFI of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) on ILC2s. E Comparison of MFI of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) on ILC3s. Error bars represent ± SD. Statistical significance was determined by one-way ANOVA (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001)

Article Snippet: Human glioma U87-MG and its isogenic IDH1 (R132H)-mutant U87-MG (#HTB14IG) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Mutagenesis, Flow Cytometry, Control, Comparison, Fluorescence, Expressing

Journal: Inflammation Research

Article Title: IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression

doi: 10.1007/s00011-026-02223-8

Figure Lengend Snippet: The frequency of ILC3 is increased in the peripheral blood of IDH1-mutant glioma patients compared with the IDH1-wild-type group. A Representative flow-cytometry gating strategies for ILCs in peripheral blood of healthy controls, IDH1-wild-type glioma patients, and IDH1-mutant glioma patients (FSC-A = forward-scatter area; SSC-A = side-scatter area). B Comparison of total ILC percentages in blood samples from healthy controls (HC, n = 20), IDH1-wild-type (n = 12), and IDH1-mutant (n = 7) groups (top center); comparison of ILC1 (bottom left), ILC2 (bottom center), and ILC3 (bottom right) frequencies across the same groups. C Comparison of MFI of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) on ILC1s in HC, IDH1-wild-type, and IDH1-mutant groups. D Comparison of MFI of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) on ILC2s. E Comparison of MFI of KLRG1 (top left), PD-1 (top right), and CTLA-4 (bottom center) on ILC3s. Error bars represent ± SD. Statistical significance was determined by one-way ANOVA (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001)

Article Snippet: Human glioma U87-MG and its isogenic IDH1 (R132H)-mutant U87-MG (#HTB14IG) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Mutagenesis, Flow Cytometry, Comparison

Journal: Inflammation Research

Article Title: IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression

doi: 10.1007/s00011-026-02223-8

Figure Lengend Snippet: Co-culture of tonsil-derived ILCs with U87-MG significantly increased surface PD-1, KLRG1, and CTLA-4 compared with IDH1-mutant U87-MG. A – D Human tonsil-derived ILCs were cultured alone or co-cultured with U87-MG or IDH1-mutant U87-MG glioma cell lines, either with cytokine supplementation (recombinant human IL-2 [5 ng/mL], IL-7 [50 ng/mL], IL-12 [50 ng/mL], IL-1β [50 ng/mL], IL-23 [50 ng/mL]) or without cytokines for four days. Data points represent two independent experiments (ILC n = 3; U87-MG + ILC n = 6; IDH1-mutant U87-MG + ILC n = 6; technical replicates) A Representative flow-cytometry gating strategy for human tonsil-derived ILCs. B Flow-cytometry contour plots showing CTLA-4, KLRG1, and PD-1 surface expression percentages on ILCs. C Quantification of CTLA-4, KLRG1, and PD-1 expression percentages on ILCs. D Mean fluorescence intensity (MFI) of CTLA-4, KLRG1, and PD-1 expression on ILCs. E – F ILCs were cultured alone or exposed to glioma-conditioned medium (GCM) from U87-MG or IDH1-mutant U87-MG cell lines under the same cytokine conditions for four days. Data points represent two independent experiments (each with three technical replicates). E Percentages of CTLA-4, KLRG1, and PD-1–expressing ILCs following GCM exposure. F Corresponding MFI of CTLA-4, KLRG1, and PD-1 expression on ILCs. G – H Proliferation of CFSE-labeled tonsil ILCs co-cultured with U87-MG or IDH1-mutant U87-MG cells was analyzed after four days. G Representative flow-cytometry plots of CFSE dilution. H Quantification of proliferating CFSE-labeled ILCs from three independent experiments (each with four technical replicates). Error bars represent ± SD. Statistical analyses were performed using one-way ANOVA (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001)

Article Snippet: Human glioma U87-MG and its isogenic IDH1 (R132H)-mutant U87-MG (#HTB14IG) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Co-Culture Assay, Derivative Assay, Mutagenesis, Cell Culture, Recombinant, Flow Cytometry, Expressing, Fluorescence, Labeling

Journal: Inflammation Research

Article Title: IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression

doi: 10.1007/s00011-026-02223-8

Figure Lengend Snippet: IL-17 and IFN-γ production is increased in tonsil-derived ILCs exposed to glioma-conditioned medium (GCM) from U87-MG and IDH1-mutant U87-MG cell lines. A – E Tonsil-derived ILCs were cultured alone or with glioma-conditioned medium (GCM) obtained from U87-MG or IDH1-mutant U87-MG cell lines for four days, with or without cytokine supplementation (recombinant human IL-2 [5 ng/mL], IL-7 [50 ng/mL], IL-12 [50 ng/mL], IL-1β [50 ng/mL], IL-23 [50 ng/mL]). Golgi Stop was added during the final nine hours of incubation. A Percentages (left) and mean fluorescence intensity (MFI; right) of TNF-α–producing ILCs. B Percentages (left) and MFI (right) of IL-2–producing ILCs. C Percentages (left) and MFI (right) of IL-17–producing ILCs. D Percentages (left) and MFI (right) of IFN-γ–producing ILCs. E Percentages (left) and MFI (right) of GM-CSF–producing ILCs. Data represents two independent experiments (each with three technical replicates). Error bars indicate ± SEM. Statistical significance was determined by one-way ANOVA (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001)

Article Snippet: Human glioma U87-MG and its isogenic IDH1 (R132H)-mutant U87-MG (#HTB14IG) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Derivative Assay, Mutagenesis, Cell Culture, Recombinant, Incubation, Fluorescence

Journal: Inflammation Research

Article Title: IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression

doi: 10.1007/s00011-026-02223-8

Figure Lengend Snippet: D-2-HG levels are comparable in-patient plasma but elevated in glioma-conditioned medium (GCM) from IDH1-mutant U87-MG + ILC co-cultures compared with U87-MG + ILC. A Quantification of D-2-HG (OD₄₅₀) in plasma samples from healthy controls (HC, n = 12), IDH1-wild-type glioma patients (n = 12), and IDH1-mutant glioma patients (n = 7). B Quantification of D-2-HG (OD₄₅₀) in glioma-conditioned medium (GCM) collected from cultures of ILCs alone, U87-MG, IDH1-mutant U87-MG cell lines, and tonsil ILCs co-cultured with U87-MG or IDH1-mutant U87-MG cells under cytokine-supplemented (recombinant human IL-2 [5 ng/mL], IL-7 [50 ng/mL], IL-12 [50 ng/mL], IL-1β [50 ng/mL], IL-23 [50 ng/mL]) and cytokine-free conditions for four days. Data points represent two independent experiments (ILC n = 4, U87-MG + ILC n = 2, IDH1-mutant U87-MG + ILC n = 2 technical replicates). Error bars indicate ± SEM. (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001)

Article Snippet: Human glioma U87-MG and its isogenic IDH1 (R132H)-mutant U87-MG (#HTB14IG) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Clinical Proteomics, Mutagenesis, Cell Culture, Recombinant

Journal: International Journal of Molecular Sciences

Article Title: EGFR-Targeted Pentacyclic Triterpene Analogues for Glioma Therapy

doi: 10.3390/ijms222010945

Figure Lengend Snippet: The cytotoxic effects of the compounds on U251, T98G, U87, and Jurkat cells, PBMCs.

Article Snippet: U251, T98G (Japanese Collection of Research Bioresources Cell Bank), and U87 human glioblastoma cell lines were incubated in Dulbecco’s Modified Eagle Medium (DMEM)/Ham’s F12 (Wako Pure Chemical Industries, Osaka, Japan), Eagle’s Minimum Essential Medium (EMEM; Wako Pure Chemical Industries, Osaka, Japan), and DMEM (Gibco/Thermo Fisher Scientific, Waltham, MA, USA) respectively, and supplemented with 10% fetal bovine serum (FBS; Sigma Aldrich, MO, USA).

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: EGFR-Targeted Pentacyclic Triterpene Analogues for Glioma Therapy

doi: 10.3390/ijms222010945

Figure Lengend Snippet: The anticancer effects of compounds 4, 10, 13, and cisplatin at varying concentrations on U251 cells ( a ), T98G cells ( b ), U87 cells ( c ), Jurkat cells ( d ), and PBMCs ( e ). All descriptive data were expressed as the mean ± standard deviation (SD). All experiments were repeated three times.

Article Snippet: U251, T98G (Japanese Collection of Research Bioresources Cell Bank), and U87 human glioblastoma cell lines were incubated in Dulbecco’s Modified Eagle Medium (DMEM)/Ham’s F12 (Wako Pure Chemical Industries, Osaka, Japan), Eagle’s Minimum Essential Medium (EMEM; Wako Pure Chemical Industries, Osaka, Japan), and DMEM (Gibco/Thermo Fisher Scientific, Waltham, MA, USA) respectively, and supplemented with 10% fetal bovine serum (FBS; Sigma Aldrich, MO, USA).

Techniques: Standard Deviation