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ifn γ e el h0108 levels  (Elabscience Biotechnology)


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    Elabscience Biotechnology ifn γ e el h0108 levels
    Ifn γ E El H0108 Levels, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 161 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 161 article reviews
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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Elevated IgG levels induce an M2‑to‑M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas.
    Article Snippet: .. Human IFN‐γ, il‐1β, il‐6, il‐10, TGF‐β and TNF‐α levels were quantified using commercial ELISA kits (Human IFN‐γ eliSa kit, cat. no. e‐el‐H0108; Human il‐1β eliSa kit, cat. no. e‐el‐H0149; Human il‐6 eliSa kit, cat. no. e‐el‐H0102; Human il‐10 ELISA kit, cat. no. E‐EL‐H0103; Human TGF‐β eliSa kit, cat. no. E‐EL‐H0110; Human TNF‐α eliSa kit, cat. no. e‐el‐H0109; Wuhan elabscience Biotechnology co., Ltd.). ..

    Article Title: Multiomics profiling Identifies MCMBP as a prognostic biomarker and a potential immune-related target in pancreatic ductal adenocarcinoma via the JAK–STAT3 pathway
    Article Snippet: After a 2 hour stabilization period, T-cell activation was induced by adding soluble anti-CD3 antibody (2μg/mL, Elabscience, Wuhan, CN), soluble anti-CD28 antibody (1μg/mL, Elabscience, Wuhan, CN), and Goat Anti-Mouse IgG (5μg/mL, Elabscience, Wuhan, CN) to the culture medium. .. Following 24 hours of activation, the cell culture supernatant was collected, and the concentration of secreted IFN-γ was quantified using a Human IFN-γ ELISA Kit (Elabscience, Wuhan, CN) according to the manufacturer’s instructions. ..

    Article Title: Knockdown of PELI1 promotes Th2 and Treg cell differentiation in juvenile idiopathic arthritis.
    Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

    Article Title: GB20-5A8-31, an anti-TL1A antibody for treating inflammatory bowel disease
    Article Snippet: .. And the IFN-γ levels were quantified using a human IFN-γ ELISA kit (Elabscience, #E-EL-H0108) according to the manufacturer’s protocol. ..

    Article Title: SREBF2 enhances lipid metabolism and represses anti-tumor immune responses in cervical cancer by increasing ACAT2
    Article Snippet: .. The cell culture medium of the co-culture system of CC cells and immune cells, or the medium of CC cells alone, was collected and centrifuged at 4 °C, 1000 × g for 20 min. Cytokine levels in the supernatant were detected by human IFN-γ ELISA Kit (E-EL-H0108, Elabscience, Wuhan, Hubei, China), human GZMB ELISA Kit (E-EL-H1617, Elabscience), and human TGF-β1 ELISA Kit (PT880, Beyotime). ..

    Article Title: Lidocaine Modulates Cytokine Production and Reprograms the Tumor Immune Microenvironment to Enhance Anti-Tumor Immune Responses in Gastric Cancer
    Article Snippet: .. The production of IFN-γ, IL-12, IL-10, and TGF-β was analyzed by the human IL-10 ELISA kit (Arigo Biolaboratories, Taipei, Taiwan), human IL-12, TGF-β ELISA kit (Elabscience, Houston, TX, USA), and human IFN-γ ELISA KIT (Gen-Probe, San Diego, CA, USA), respectively. ..

    Article Title: Chrysin Enhances Anti-Cancer Activity of Jurkat T Cell and NK-92 Cells Against Human Breast Cancer Cell Lines.
    Article Snippet: Chrysin, a naturally occurring flavonoid in plant and bee products, demonstrates notable biological activities, including anti-cancer effects.. These properties are partially attributed to its capability to activate immune cells.. This study focused on exploring the immunomodulatory potential of chrysin on NK-92 and Jurkat-T cells targeting breast cancer cells (BCC).

    Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas
    Article Snippet: .. Human IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α levels were quantified using commercial ELISA kits (Human IFN-γ ELISA kit, cat. no. E-EL-H0108; Human IL-1β ELISA kit, cat. no. E-EL-H0149; Human IL-6 ELISA kit, cat. no. E-EL-H0102; Human IL-10 ELISA kit, cat. no. E-EL-H0103; Human TGF-β ELISA kit, cat. no. E-EL-H0110; Human TNF-α ELISA kit, cat. no. E-EL-H0109; Wuhan Elabscience Biotechnology Co., Ltd.). ..

    Activation Assay:

    Article Title: Multiomics profiling Identifies MCMBP as a prognostic biomarker and a potential immune-related target in pancreatic ductal adenocarcinoma via the JAK–STAT3 pathway
    Article Snippet: After a 2 hour stabilization period, T-cell activation was induced by adding soluble anti-CD3 antibody (2μg/mL, Elabscience, Wuhan, CN), soluble anti-CD28 antibody (1μg/mL, Elabscience, Wuhan, CN), and Goat Anti-Mouse IgG (5μg/mL, Elabscience, Wuhan, CN) to the culture medium. .. Following 24 hours of activation, the cell culture supernatant was collected, and the concentration of secreted IFN-γ was quantified using a Human IFN-γ ELISA Kit (Elabscience, Wuhan, CN) according to the manufacturer’s instructions. ..

    Cell Culture:

    Article Title: Multiomics profiling Identifies MCMBP as a prognostic biomarker and a potential immune-related target in pancreatic ductal adenocarcinoma via the JAK–STAT3 pathway
    Article Snippet: After a 2 hour stabilization period, T-cell activation was induced by adding soluble anti-CD3 antibody (2μg/mL, Elabscience, Wuhan, CN), soluble anti-CD28 antibody (1μg/mL, Elabscience, Wuhan, CN), and Goat Anti-Mouse IgG (5μg/mL, Elabscience, Wuhan, CN) to the culture medium. .. Following 24 hours of activation, the cell culture supernatant was collected, and the concentration of secreted IFN-γ was quantified using a Human IFN-γ ELISA Kit (Elabscience, Wuhan, CN) according to the manufacturer’s instructions. ..

    Article Title: SREBF2 enhances lipid metabolism and represses anti-tumor immune responses in cervical cancer by increasing ACAT2
    Article Snippet: .. The cell culture medium of the co-culture system of CC cells and immune cells, or the medium of CC cells alone, was collected and centrifuged at 4 °C, 1000 × g for 20 min. Cytokine levels in the supernatant were detected by human IFN-γ ELISA Kit (E-EL-H0108, Elabscience, Wuhan, Hubei, China), human GZMB ELISA Kit (E-EL-H1617, Elabscience), and human TGF-β1 ELISA Kit (PT880, Beyotime). ..

    Concentration Assay:

    Article Title: Multiomics profiling Identifies MCMBP as a prognostic biomarker and a potential immune-related target in pancreatic ductal adenocarcinoma via the JAK–STAT3 pathway
    Article Snippet: After a 2 hour stabilization period, T-cell activation was induced by adding soluble anti-CD3 antibody (2μg/mL, Elabscience, Wuhan, CN), soluble anti-CD28 antibody (1μg/mL, Elabscience, Wuhan, CN), and Goat Anti-Mouse IgG (5μg/mL, Elabscience, Wuhan, CN) to the culture medium. .. Following 24 hours of activation, the cell culture supernatant was collected, and the concentration of secreted IFN-γ was quantified using a Human IFN-γ ELISA Kit (Elabscience, Wuhan, CN) according to the manufacturer’s instructions. ..

    Article Title: Knockdown of PELI1 promotes Th2 and Treg cell differentiation in juvenile idiopathic arthritis.
    Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.



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    MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, <t>IFN-γ,</t> LPS, and NGF were detected by <t>ELISA</t> after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) <t>ELISA</t> of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.
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    MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, <t>IFN-γ,</t> LPS, and NGF were detected by <t>ELISA</t> after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) <t>ELISA</t> of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.
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    Image Search Results


    MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, IFN-γ, LPS, and NGF were detected by ELISA after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) ELISA of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.

    Journal: Cell Reports Medicine

    Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

    doi: 10.1016/j.xcrm.2026.102937

    Figure Lengend Snippet: MSM-DTM adsorbs inflammatory cytokines, suppresses TSPCs inflammation and senescence, and promotes tenogenic differentiation and migration (A) The remaining concentrations of TNF-α, IL-1β, IL-6, IFN-γ, LPS, and NGF were detected by ELISA after co-culture with different concentrations of MSM. (B and C) RT-qPCR of IL-6 and CCL-2 in TSPCs under different treatments. (D) Western blot of COL1A2, MMP3, and TNMD. (E) ELISA of TNF-α, IL-6, and IFN-γ in supernatants. (F)Western blot of p16 and p21 after 7 days of treatment. (G) β-Galactosidase staining analysis after 7 days of treatment. Scale bars, 100 μm. (H and I) Immunofluorescence and quantification of TNMD and TNC after 14-day treatment. Scale bars, 50 μm. (J) Relative mRNA expression of tenogenic differentiation markers SCX and TNC. (K and L) Representative images and quantification of Transwell assay. Scale bars, 100 μm. (M and N) Representative images and quantification of wound healing assay. Scale bars, 100 μm. Statistical comparisons were performed with one-way ANOVA with Tukey’s multiple comparisons test. Data are presented as the mean ± SD, n = 3. Ns, no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 between groups.

    Article Snippet: IFN-γ ELISA kit , ABclonal , RK00015.

    Techniques: Migration, Enzyme-linked Immunosorbent Assay, Co-Culture Assay, Quantitative RT-PCR, Western Blot, Staining, Immunofluorescence, Expressing, Transwell Assay, Wound Healing Assay

    Journal: Cell Reports Medicine

    Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

    doi: 10.1016/j.xcrm.2026.102937

    Figure Lengend Snippet:

    Article Snippet: IFN-γ ELISA kit , ABclonal , RK00015.

    Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

    Vectorized IFNβ drives durable signaling and complete tumor regression in human glioblastoma models in vivo (A) Sustained hIFNβ secretion in human GBM6 cells treated with AAV9-hIFNβ (red, MOI = 4E5 vg/cell) or recombinant hIFNβ cytokine (r-hIFNβ, purple, 47 IU/mL, equivalent to 114 pg/mL), measured by ELISA at indicated time points. 50% media washouts every 5 h for the first 20 h in the r-hIFNβ condition mimic in vivo cytokine clearance (half-life = 4–5 h). Full media exchanges were performed at 24, 48, 72, and 96 h post-treatment. (B) Number of differentially expressed genes (DEGs, p -Adj<0.01) in GBM6 cells 24–96 h post-treatment with AAV9-hIFNβ or r-hIFNβ vs. media controls. (C) Enrichment scores for type I IFN and TNFα response pathways across treatments and time points. (D) Heatmap of the top 10 IFN and TNFα response genes (Log2FC vs. media controls) in GBM6 cells treated as in (A). (E) Schematic of orthotopic PDX (SF11411) and cell line-derived xenograft ([CDX], GBM6-FLuc) studies in athymic nu/nu mice treated intratumorally with saline, AAV9-GFP, or AAV9-hIFNβ via CED. (F) Kaplan-Meier survival curves for PDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Vertical dashed line = day of treatment (day 9). p < 0.04 by log-rank (Mantel-Cox) test. n = 30 (10 per treatment arm). (G) Longitudinal BLI of GBM6-FLuc tumor growth in CDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗ p < 0.04 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 22. n = 30 (10 per treatment arm). (G′) Representative BLI images from each treatment group 11 days post-treatment. (H) Kaplan-Meier survival curves for CDX mice. p < 0.001 by log-rank (Mantel-Cox) test. (I) Distribution of treatment responses in CDX by BLI flux (photons/second) at day 27. Tumor free = BLI flux <2.5 × 10 5 p/s, tumor reduction = ≥30% decrease from assignment on day 9, no change = between 30% decrease and 20% increase from assignment on day 9, tumor growth = ≥20% increase from assignment on day 9, death = mice that died before day 27. (J) Dose-response analysis of AAV9-hIFNβ efficacy in CDX mice. AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ hi (2E11 vg/brain) = solid red, and AAV9-hIFNβ lo (1E11 vg/brain) = dashed red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗∗ p < 0.02 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 20. n = 45 (15 per treatment arm). For data interpretation, tumor burden threshold = 2.5 × 10 5 . (J′) Representative BLI images of tumors 11 days post-treatment. (K) Kaplan-Meier survival curves from (J). p < 0.002 (AAV9-hIFNβ hi), p < 0.005 (AAV9-hIFNβ lo) by log-rank (Mantel-Cox) test compared to AAV9-GFP. (I) Distribution of treatment responses in CDX mice at day 27 by BLI flux as in (I).

    Journal: Molecular Therapy Oncology

    Article Title: AAV immuno-gene therapy platform delivering vectorized cytokines defines a new modality for high-grade glioma treatment

    doi: 10.1016/j.omton.2026.201183

    Figure Lengend Snippet: Vectorized IFNβ drives durable signaling and complete tumor regression in human glioblastoma models in vivo (A) Sustained hIFNβ secretion in human GBM6 cells treated with AAV9-hIFNβ (red, MOI = 4E5 vg/cell) or recombinant hIFNβ cytokine (r-hIFNβ, purple, 47 IU/mL, equivalent to 114 pg/mL), measured by ELISA at indicated time points. 50% media washouts every 5 h for the first 20 h in the r-hIFNβ condition mimic in vivo cytokine clearance (half-life = 4–5 h). Full media exchanges were performed at 24, 48, 72, and 96 h post-treatment. (B) Number of differentially expressed genes (DEGs, p -Adj<0.01) in GBM6 cells 24–96 h post-treatment with AAV9-hIFNβ or r-hIFNβ vs. media controls. (C) Enrichment scores for type I IFN and TNFα response pathways across treatments and time points. (D) Heatmap of the top 10 IFN and TNFα response genes (Log2FC vs. media controls) in GBM6 cells treated as in (A). (E) Schematic of orthotopic PDX (SF11411) and cell line-derived xenograft ([CDX], GBM6-FLuc) studies in athymic nu/nu mice treated intratumorally with saline, AAV9-GFP, or AAV9-hIFNβ via CED. (F) Kaplan-Meier survival curves for PDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Vertical dashed line = day of treatment (day 9). p < 0.04 by log-rank (Mantel-Cox) test. n = 30 (10 per treatment arm). (G) Longitudinal BLI of GBM6-FLuc tumor growth in CDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗ p < 0.04 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 22. n = 30 (10 per treatment arm). (G′) Representative BLI images from each treatment group 11 days post-treatment. (H) Kaplan-Meier survival curves for CDX mice. p < 0.001 by log-rank (Mantel-Cox) test. (I) Distribution of treatment responses in CDX by BLI flux (photons/second) at day 27. Tumor free = BLI flux <2.5 × 10 5 p/s, tumor reduction = ≥30% decrease from assignment on day 9, no change = between 30% decrease and 20% increase from assignment on day 9, tumor growth = ≥20% increase from assignment on day 9, death = mice that died before day 27. (J) Dose-response analysis of AAV9-hIFNβ efficacy in CDX mice. AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ hi (2E11 vg/brain) = solid red, and AAV9-hIFNβ lo (1E11 vg/brain) = dashed red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗∗ p < 0.02 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 20. n = 45 (15 per treatment arm). For data interpretation, tumor burden threshold = 2.5 × 10 5 . (J′) Representative BLI images of tumors 11 days post-treatment. (K) Kaplan-Meier survival curves from (J). p < 0.002 (AAV9-hIFNβ hi), p < 0.005 (AAV9-hIFNβ lo) by log-rank (Mantel-Cox) test compared to AAV9-GFP. (I) Distribution of treatment responses in CDX mice at day 27 by BLI flux as in (I).

    Article Snippet: 24, 48, 72, and 96 h after treatment, cell supernatants were collected and IFN variant levels were measured using IFN ELISA kits following the manufacturer’s instructions (human IFNα [PBL Cat# 41135-1], human IFNβ [PBL Cat#41410], and human IFNγ [R&D Systems Cat#: DIF50C]).

    Techniques: In Vivo, Recombinant, Enzyme-linked Immunosorbent Assay, Derivative Assay, Saline

    Spatial transcriptomics reveals rapid, localized transcriptional remodeling of the tumor microenvironment following vectorized hIFNβ treatment (A) Coronal brain sections from representative human GBM6-FLuc CDX mice collected pre-treatment (0 h, n = 1) or 48 h ( n = 1) after intratumoral AAV9-hIFNβ infusion (2E11 vg/brain), stained with H&E (left) and subjected to Visium Spatial Gene Expression profiling (right). Annotated clusters were assigned based on anatomical localization and marker gene expression. Dashed lines denote tumor borders. Scale bars, 1 mm. (B) Top 10 marker genes for each spatially resolved cluster identified across 0 h and 48 h datasets. Values are shown as log-normalized expression centered at 0 (Seurat “scale.data”). (C) Spatial expression of canonical human GBM tumor markers ( CD44 , VIM , TOP2A , and NOTCH1 ) delineating tumor and peri-tumor regions before (0 h) (top) and after (bottom) (48 h) AAV9-hIFNβ treatment. (D) Expression maps of the human IFNβ payload and hallmark IFN-response genes ( CXCL10 , IFIT1 , and IFIT2 ), demonstrating tumor-restricted transgene expression and induction of an IFN-specific transcriptional program within 48 h. (E) Spatial expression of host mouse immune-response genes ( Gfap , Ifitm3 , and Irf7 ) showing localized activation of astroglial and innate immune pathways proximal to the tumor. (F) Integrated datasets (0 and 48 h) visualized using canonical correlation analysis (CCA), showing distinct clustering of tumor and peri-tumor regions (left) and enrichment of IFN-response gene module expression (right). (G) Volcano plot depicting differential gene expression between 0- and 48-h tumor clusters. Red, IFN-response genes; gray, other significantly upregulated genes ( p -Adj <0.01); blue, non-significant. (H) Top enriched Gene Ontology (GO) terms among upregulated genes in 48-h tumor cells, highlighting interferon and inflammatory response pathways (∗∗ p -Adj <0.01; ∗ p -Adj <0.05).

    Journal: Molecular Therapy Oncology

    Article Title: AAV immuno-gene therapy platform delivering vectorized cytokines defines a new modality for high-grade glioma treatment

    doi: 10.1016/j.omton.2026.201183

    Figure Lengend Snippet: Spatial transcriptomics reveals rapid, localized transcriptional remodeling of the tumor microenvironment following vectorized hIFNβ treatment (A) Coronal brain sections from representative human GBM6-FLuc CDX mice collected pre-treatment (0 h, n = 1) or 48 h ( n = 1) after intratumoral AAV9-hIFNβ infusion (2E11 vg/brain), stained with H&E (left) and subjected to Visium Spatial Gene Expression profiling (right). Annotated clusters were assigned based on anatomical localization and marker gene expression. Dashed lines denote tumor borders. Scale bars, 1 mm. (B) Top 10 marker genes for each spatially resolved cluster identified across 0 h and 48 h datasets. Values are shown as log-normalized expression centered at 0 (Seurat “scale.data”). (C) Spatial expression of canonical human GBM tumor markers ( CD44 , VIM , TOP2A , and NOTCH1 ) delineating tumor and peri-tumor regions before (0 h) (top) and after (bottom) (48 h) AAV9-hIFNβ treatment. (D) Expression maps of the human IFNβ payload and hallmark IFN-response genes ( CXCL10 , IFIT1 , and IFIT2 ), demonstrating tumor-restricted transgene expression and induction of an IFN-specific transcriptional program within 48 h. (E) Spatial expression of host mouse immune-response genes ( Gfap , Ifitm3 , and Irf7 ) showing localized activation of astroglial and innate immune pathways proximal to the tumor. (F) Integrated datasets (0 and 48 h) visualized using canonical correlation analysis (CCA), showing distinct clustering of tumor and peri-tumor regions (left) and enrichment of IFN-response gene module expression (right). (G) Volcano plot depicting differential gene expression between 0- and 48-h tumor clusters. Red, IFN-response genes; gray, other significantly upregulated genes ( p -Adj <0.01); blue, non-significant. (H) Top enriched Gene Ontology (GO) terms among upregulated genes in 48-h tumor cells, highlighting interferon and inflammatory response pathways (∗∗ p -Adj <0.01; ∗ p -Adj <0.05).

    Article Snippet: 24, 48, 72, and 96 h after treatment, cell supernatants were collected and IFN variant levels were measured using IFN ELISA kits following the manufacturer’s instructions (human IFNα [PBL Cat# 41135-1], human IFNβ [PBL Cat#41410], and human IFNγ [R&D Systems Cat#: DIF50C]).

    Techniques: Spatial Transcriptomics, Staining, Gene Expression, Marker, Expressing, Activation Assay

    IFN-γ suppresses tumor growth and invasion. (A) Cytokine profiling of co-culture supernatants via ELISAs: IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α. (B-D) Spatial expression patterns of IFN-γ. (B) Immunofluorescence imaging of the invasive front in SSIT, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green), and grayscale intensity distribution. (C) Immunofluorescence imaging of TIM and NIM, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green). (D) Quantification of relative IFN-γ expression in TIM and NIM. (E) Representative Ki-67 immunohistochemistry images of SSIT cases stratified into IFN-γ-high and IFN-γ-low groups (n=5 each; median split). (F) Quantification of Ki-67 index comparing the two groups. (G) EdU staining demonstrating dose-dependent suppression of TtT/GF pituitary adenoma cell proliferation by IFN-γ (0–100 ng/ml; 48 h). (H) Representative flow cytometry histograms for cell cycle analysis of cells treated with IFN-γ (0–100 ng/ml) in the absence (0 µM) or presence (5 µM) of ruxolitinib. (I) Stacked bar plot showing the percentages of cells in the G 1 , S and G 2 /M phases under the same treatment conditions. (A) One-way ANOVA with Tukey's post hoc multiple comparisons test. (D and F) Unpaired two-tailed Student's t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. CTRL, control; DMC, digested mucosal culture; EdU, 5-ethynyl-2′-deoxyuridine; IBA-1, ionised calcium binding adaptor molecule 1; MTC, mucosal tissue culture; NIM, non-invaded mucosa; ns, not significant; PE-A, phycoerythrin-area; SSIT, sphenoid sinus-invasive tumor; TIM, tumor-invaded mucosa.

    Journal: Molecular Medicine Reports

    Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

    doi: 10.3892/mmr.2026.13878

    Figure Lengend Snippet: IFN-γ suppresses tumor growth and invasion. (A) Cytokine profiling of co-culture supernatants via ELISAs: IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α. (B-D) Spatial expression patterns of IFN-γ. (B) Immunofluorescence imaging of the invasive front in SSIT, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green), and grayscale intensity distribution. (C) Immunofluorescence imaging of TIM and NIM, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green). (D) Quantification of relative IFN-γ expression in TIM and NIM. (E) Representative Ki-67 immunohistochemistry images of SSIT cases stratified into IFN-γ-high and IFN-γ-low groups (n=5 each; median split). (F) Quantification of Ki-67 index comparing the two groups. (G) EdU staining demonstrating dose-dependent suppression of TtT/GF pituitary adenoma cell proliferation by IFN-γ (0–100 ng/ml; 48 h). (H) Representative flow cytometry histograms for cell cycle analysis of cells treated with IFN-γ (0–100 ng/ml) in the absence (0 µM) or presence (5 µM) of ruxolitinib. (I) Stacked bar plot showing the percentages of cells in the G 1 , S and G 2 /M phases under the same treatment conditions. (A) One-way ANOVA with Tukey's post hoc multiple comparisons test. (D and F) Unpaired two-tailed Student's t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. CTRL, control; DMC, digested mucosal culture; EdU, 5-ethynyl-2′-deoxyuridine; IBA-1, ionised calcium binding adaptor molecule 1; MTC, mucosal tissue culture; NIM, non-invaded mucosa; ns, not significant; PE-A, phycoerythrin-area; SSIT, sphenoid sinus-invasive tumor; TIM, tumor-invaded mucosa.

    Article Snippet: Human IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α levels were quantified using commercial ELISA kits (Human IFN-γ ELISA kit, cat. no. E-EL-H0108; Human IL-1β ELISA kit, cat. no. E-EL-H0149; Human IL-6 ELISA kit, cat. no. E-EL-H0102; Human IL-10 ELISA kit, cat. no. E-EL-H0103; Human TGF-β ELISA kit, cat. no. E-EL-H0110; Human TNF-α ELISA kit, cat. no. E-EL-H0109; Wuhan Elabscience Biotechnology Co., Ltd.).

    Techniques: Co-Culture Assay, Expressing, Immunofluorescence, Imaging, Immunohistochemistry, Staining, Flow Cytometry, Cell Cycle Assay, Two Tailed Test, Control, Binding Assay

    Elevated IgG levels drive macrophage M2-to-M1 reprogramming. (A) Sphenoid sinus-invasive tumor cases stratified into CD19-high (n=5) and CD19-low (n=5) groups based on the cohort median of CD19 + B cell density, with (B) quantitative analyses of macrophage polarization (M1-like versus M2-like). (C) Dural-invasive tumor and non-invasive tumor cases stratified into IgG-high (n=27) and IgG-low (n=26) groups based on the cohort median of relative IgG immunohistochemistry staining intensity, with (D) quantitative analyses of M1-like/M2-like macrophage proportions. (E and F) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by IgG (10 µg/ml) exposure. Relative (E) IL-6 and (F) TNF-α mRNA expression in RAW264.7 macrophages pre-polarized to M0, M1 or M2 states. (G) Representative flow cytometric cell-cycle profiles of TtT/GF cells following the indicated treatments. (H) Stacked bar plot summarizing the percentages of cells from (G) in G 1 , S and G 2 /M phases. (I) Representative images from the scratch wound assay at 0, 24, 48 and 72 h under the indicated treatments. (J) Quantification of scratch wound closure. (K) Representative western blot images showing total STAT1, p-STAT1, total STAT3, p-STAT3 and β-actin levels in cells treated with IFN-γ (100 ng/ml), IL-6 (100 ng/ml), IFN-γ + IL-6 (50 ng/ml each), ruxolitinib (5 µM) or IFN-γ + IL-6 (50 ng/ml each) plus ruxolitinib (5 µM), as indicated. (L) Densitometric semi-quantification of p-STAT1/STAT1 (ratio). (B and D) Unpaired two-tailed Student's t-test. (E, F, J and L) One-way ANOVA with Tukey's post hoc multiple comparisons test. *P<0.05, ***P<0.001, ****P<0.0001. CTRL, control; IBA-1, ionised calcium binding adaptor molecule 1; ns, not significant; p-, phosphorylated; PE-A, phycoerythrin-area.

    Journal: Molecular Medicine Reports

    Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

    doi: 10.3892/mmr.2026.13878

    Figure Lengend Snippet: Elevated IgG levels drive macrophage M2-to-M1 reprogramming. (A) Sphenoid sinus-invasive tumor cases stratified into CD19-high (n=5) and CD19-low (n=5) groups based on the cohort median of CD19 + B cell density, with (B) quantitative analyses of macrophage polarization (M1-like versus M2-like). (C) Dural-invasive tumor and non-invasive tumor cases stratified into IgG-high (n=27) and IgG-low (n=26) groups based on the cohort median of relative IgG immunohistochemistry staining intensity, with (D) quantitative analyses of M1-like/M2-like macrophage proportions. (E and F) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by IgG (10 µg/ml) exposure. Relative (E) IL-6 and (F) TNF-α mRNA expression in RAW264.7 macrophages pre-polarized to M0, M1 or M2 states. (G) Representative flow cytometric cell-cycle profiles of TtT/GF cells following the indicated treatments. (H) Stacked bar plot summarizing the percentages of cells from (G) in G 1 , S and G 2 /M phases. (I) Representative images from the scratch wound assay at 0, 24, 48 and 72 h under the indicated treatments. (J) Quantification of scratch wound closure. (K) Representative western blot images showing total STAT1, p-STAT1, total STAT3, p-STAT3 and β-actin levels in cells treated with IFN-γ (100 ng/ml), IL-6 (100 ng/ml), IFN-γ + IL-6 (50 ng/ml each), ruxolitinib (5 µM) or IFN-γ + IL-6 (50 ng/ml each) plus ruxolitinib (5 µM), as indicated. (L) Densitometric semi-quantification of p-STAT1/STAT1 (ratio). (B and D) Unpaired two-tailed Student's t-test. (E, F, J and L) One-way ANOVA with Tukey's post hoc multiple comparisons test. *P<0.05, ***P<0.001, ****P<0.0001. CTRL, control; IBA-1, ionised calcium binding adaptor molecule 1; ns, not significant; p-, phosphorylated; PE-A, phycoerythrin-area.

    Article Snippet: Human IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α levels were quantified using commercial ELISA kits (Human IFN-γ ELISA kit, cat. no. E-EL-H0108; Human IL-1β ELISA kit, cat. no. E-EL-H0149; Human IL-6 ELISA kit, cat. no. E-EL-H0102; Human IL-10 ELISA kit, cat. no. E-EL-H0103; Human TGF-β ELISA kit, cat. no. E-EL-H0110; Human TNF-α ELISA kit, cat. no. E-EL-H0109; Wuhan Elabscience Biotechnology Co., Ltd.).

    Techniques: Immunohistochemistry, Staining, Expressing, Scratch Wound Assay Assay, Western Blot, Two Tailed Test, Control, Binding Assay

    Anti-CD47 mAb enhances ADCP to suppress tumor cell proliferation. (A) Immunofluorescence staining of CD47 (red) and DAPI (blue) in a representative subset of non-invasive tumor, dural-invasive tumor and sphenoid sinus-invasive tumor cases (n=10 per group). (B) Paired comparison of CD47 fluorescence intensity at the IF versus the TC. (C) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by anti-CD47 mAb (10 µg/ml) treatment for 12 h. Quantitative PCR was used to analyze polarization/activation markers. (D) Schematic illustrating anti-CD47 mAb-mediated blockade of the CD47-SIRPα axis and enhancement of ADCP. (E) EdU assay of TtT/GF cell proliferation in a Transwell co-culture with anti-CD47 mAb-treated polarized macrophages. (F) Quantification of EdU-positive cells. (G) Representative microscopy images and flow cytometry plots showing macrophage phagocytosis of pHrodo™ Red-labeled GFP-TtT/GF cells. (H) Quantification of phagocytosis (%). (B) Paired two-tailed Student's t-test. (C, F and H) One-way ANOVA with Tukey's post hoc multiple comparisons test. **P<0.01, ***P<0.001, ****P<0.0001. ADCP, antibody-dependent cellular phagocytosis; Arg-1, arginase 1; EdU, 5-ethynyl-2′-deoxyuridine; FcγR, Fcγ receptor; GFP, green fluorescent protein; IF, invasive front; mAb, monoclonal antibody; NOS2, nitric oxide synthase 2; ns, not significant; PE, phycoerythrin; SIRPα, signal regulatory protein-α; SSCA, side scatter area; TC, tumor core.

    Journal: Molecular Medicine Reports

    Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

    doi: 10.3892/mmr.2026.13878

    Figure Lengend Snippet: Anti-CD47 mAb enhances ADCP to suppress tumor cell proliferation. (A) Immunofluorescence staining of CD47 (red) and DAPI (blue) in a representative subset of non-invasive tumor, dural-invasive tumor and sphenoid sinus-invasive tumor cases (n=10 per group). (B) Paired comparison of CD47 fluorescence intensity at the IF versus the TC. (C) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by anti-CD47 mAb (10 µg/ml) treatment for 12 h. Quantitative PCR was used to analyze polarization/activation markers. (D) Schematic illustrating anti-CD47 mAb-mediated blockade of the CD47-SIRPα axis and enhancement of ADCP. (E) EdU assay of TtT/GF cell proliferation in a Transwell co-culture with anti-CD47 mAb-treated polarized macrophages. (F) Quantification of EdU-positive cells. (G) Representative microscopy images and flow cytometry plots showing macrophage phagocytosis of pHrodo™ Red-labeled GFP-TtT/GF cells. (H) Quantification of phagocytosis (%). (B) Paired two-tailed Student's t-test. (C, F and H) One-way ANOVA with Tukey's post hoc multiple comparisons test. **P<0.01, ***P<0.001, ****P<0.0001. ADCP, antibody-dependent cellular phagocytosis; Arg-1, arginase 1; EdU, 5-ethynyl-2′-deoxyuridine; FcγR, Fcγ receptor; GFP, green fluorescent protein; IF, invasive front; mAb, monoclonal antibody; NOS2, nitric oxide synthase 2; ns, not significant; PE, phycoerythrin; SIRPα, signal regulatory protein-α; SSCA, side scatter area; TC, tumor core.

    Article Snippet: Human IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α levels were quantified using commercial ELISA kits (Human IFN-γ ELISA kit, cat. no. E-EL-H0108; Human IL-1β ELISA kit, cat. no. E-EL-H0149; Human IL-6 ELISA kit, cat. no. E-EL-H0102; Human IL-10 ELISA kit, cat. no. E-EL-H0103; Human TGF-β ELISA kit, cat. no. E-EL-H0110; Human TNF-α ELISA kit, cat. no. E-EL-H0109; Wuhan Elabscience Biotechnology Co., Ltd.).

    Techniques: Immunofluorescence, Staining, Comparison, Fluorescence, Real-time Polymerase Chain Reaction, Activation Assay, EdU Assay, Co-Culture Assay, Microscopy, Flow Cytometry, Labeling, Two Tailed Test

    Summary graphic illustration. This illustration summarizes the proposed model during pituitary adenoma invasion. The tumor invasive front abuts an intact sphenoid sinus mucosa, forming a distinct boundary. The mucosal compartment is enriched for ionised calcium binding adaptor molecule 1-positive macrophages with an M1-like predominance and IgG-high B cells. B cell-derived IgG promotes M2-to-M1 macrophage reprogramming, while coordinated IFN-γ and IL-6 production establishes a tumor-suppressive cytokine gradient that decreases from mucosa toward the tumor core, constraining proliferation and migration via JAK-STAT1 activation. Therapeutically, anti-CD47 monoclonal antibody blocks the CD47-SIRPα ‘don't-eat-me’ axis and augments antibody-dependent cellular phagocytosis, highlighting a strategy for immune checkpoint-targeted therapy that may complement surgical management. FcR, Fc receptor; JAK, Janus kinase; mAb, monoclonal antibody; p-, phosphorylated; SIRPα, signal regulatory protein-α.

    Journal: Molecular Medicine Reports

    Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

    doi: 10.3892/mmr.2026.13878

    Figure Lengend Snippet: Summary graphic illustration. This illustration summarizes the proposed model during pituitary adenoma invasion. The tumor invasive front abuts an intact sphenoid sinus mucosa, forming a distinct boundary. The mucosal compartment is enriched for ionised calcium binding adaptor molecule 1-positive macrophages with an M1-like predominance and IgG-high B cells. B cell-derived IgG promotes M2-to-M1 macrophage reprogramming, while coordinated IFN-γ and IL-6 production establishes a tumor-suppressive cytokine gradient that decreases from mucosa toward the tumor core, constraining proliferation and migration via JAK-STAT1 activation. Therapeutically, anti-CD47 monoclonal antibody blocks the CD47-SIRPα ‘don't-eat-me’ axis and augments antibody-dependent cellular phagocytosis, highlighting a strategy for immune checkpoint-targeted therapy that may complement surgical management. FcR, Fc receptor; JAK, Janus kinase; mAb, monoclonal antibody; p-, phosphorylated; SIRPα, signal regulatory protein-α.

    Article Snippet: Human IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α levels were quantified using commercial ELISA kits (Human IFN-γ ELISA kit, cat. no. E-EL-H0108; Human IL-1β ELISA kit, cat. no. E-EL-H0149; Human IL-6 ELISA kit, cat. no. E-EL-H0102; Human IL-10 ELISA kit, cat. no. E-EL-H0103; Human TGF-β ELISA kit, cat. no. E-EL-H0110; Human TNF-α ELISA kit, cat. no. E-EL-H0109; Wuhan Elabscience Biotechnology Co., Ltd.).

    Techniques: Binding Assay, Derivative Assay, Migration, Activation Assay