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circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of <t>IL-10,</t> TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.
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circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of <t>IL-10,</t> TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.
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Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and <t>IL-10,</t> and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).
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circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of <t>IL-10,</t> TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations <t>of</t> <t>IL-10</t> and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.
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circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: For mouse experiments, mouse IL-10 was measured using the Mouse IL-10 ELISA Kit (R&D Systems, Cat# M1000B), and mouse TGF-β1 was measured using the Mouse TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS608-4), following the manufacturers’ instructions.

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: Human IL-10 was quantified using IL-10 DuoSet ELISA (R&D Systems, Cat# DY217B), and human TGF-β1 was measured using the Human TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS249-4).

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and IL-10, and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).

Journal: Bioactive Materials

Article Title: Glucose/ROS-responsive and redox-gated adaptive hydrogel dressing for accelerating diabetic wound repair via synergistic cGAS/STING pathway inhibition and oxidative stress alleviation

doi: 10.1016/j.bioactmat.2026.03.025

Figure Lengend Snippet: Angiogenesis and collagen deposition in diabetic wound tissues following HPSL@SG hydrogel treatment. (A) Dihydroethidium (DHE) immunofluorescence staining and (B) semi-quantitative analysis of wound tissues from each treatment group on day 7, scale bar = 100 μm. Immunofluorescence staining of (C) MMP-9, IL-6, and IL-10, and (D) CD31, VEGF-A, and collagen I in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. (E-J) Mean relative fluorescence intensity of each indicator in wound tissue sections from each treatment group on day 7, scale bar = 100 μm. All data are shown as mean ± SEM (n = 6).

Article Snippet: IL-6 and IL-10-specific antibodies were purchased from Bosterbio (Wuhan, China).

Techniques: Immunofluorescence, Staining, Fluorescence

circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: Human IL-10 was quantified using IL-10 DuoSet ELISA (R&D Systems, Cat# DY217B), and human TGF-β1 was measured using the Human TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS249-4).

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations of IL-10 and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.

Journal: Brain, Behavior, & Immunity - Health

Article Title: Exploring the role of PD-1 as a marker in drug-refractory epilepsy and its potential indication for valproic acid treatment

doi: 10.1016/j.bbih.2026.101238

Figure Lengend Snippet: Elevated PD-1 expression and altered cytokine levels in plasma of IE patients. (A) PD-1 expression on CD4 + CD25 high Tregs is significantly increased in IE patients, particularly in the ISE subgroup, while CD4 + and CD4 + CD25 + T cell percentages are reduced. (B) Plasma concentrations of IL-10 and IL-6 are elevated in IE patients, with IL-10 showing a progressive increase with seizure severity. (C) Correlation analyses reveal associations between immune parameters and clinical characteristics. ∗∗∗P < 0.001, ∗∗ P < 0.01, ∗ P < 0.05; ns indicates not significant.

Article Snippet: Concentrations of IL-10 and IL-6 in plasma and CSF were quantified using commercial double-antibody sandwich ELISA kits (Boster Bioengineering, China), according to the manufacturer's instructions.

Techniques: Expressing, Clinical Proteomics

Central nervous system immune activation in ISE patients. (A) PD-1 + CD4 + CD25 high Treg cell counts are significantly elevated in the CSF of ISE patients compared to controls. (B) Both IL-10 and IL-6 concentrations are increased in the CSF of ISE patients. (C) Age correlates positively with PD-1 + CD4 + CD25 low and CD4 + CD25 high Treg percentages, and negatively with CD4 + T cell percentage in the CSF of ISE patients. ∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05.

Journal: Brain, Behavior, & Immunity - Health

Article Title: Exploring the role of PD-1 as a marker in drug-refractory epilepsy and its potential indication for valproic acid treatment

doi: 10.1016/j.bbih.2026.101238

Figure Lengend Snippet: Central nervous system immune activation in ISE patients. (A) PD-1 + CD4 + CD25 high Treg cell counts are significantly elevated in the CSF of ISE patients compared to controls. (B) Both IL-10 and IL-6 concentrations are increased in the CSF of ISE patients. (C) Age correlates positively with PD-1 + CD4 + CD25 low and CD4 + CD25 high Treg percentages, and negatively with CD4 + T cell percentage in the CSF of ISE patients. ∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05.

Article Snippet: Concentrations of IL-10 and IL-6 in plasma and CSF were quantified using commercial double-antibody sandwich ELISA kits (Boster Bioengineering, China), according to the manufacturer's instructions.

Techniques: Activation Assay

VPA treatment modulates PD-1 expression and IL-10 levels independently of drug concentration. (A) Plasma PD-1 expression on both CD4 + CD25 high and CD4 + CD25 low Treg subsets decreases significantly after 48 h of VPA treatment. (B) Plasma IL-10 levels decrease significantly after VPA treatment, while IL-6 shows no significant change. (C) Seizure control time correlates with immunological parameters but not with VPA concentrations. (D) VPA concentrations in CSF are significantly lower than in plasma, with no change between d0 and d3, and no correlation with seizure control time. ∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05; ns indicates not significant.

Journal: Brain, Behavior, & Immunity - Health

Article Title: Exploring the role of PD-1 as a marker in drug-refractory epilepsy and its potential indication for valproic acid treatment

doi: 10.1016/j.bbih.2026.101238

Figure Lengend Snippet: VPA treatment modulates PD-1 expression and IL-10 levels independently of drug concentration. (A) Plasma PD-1 expression on both CD4 + CD25 high and CD4 + CD25 low Treg subsets decreases significantly after 48 h of VPA treatment. (B) Plasma IL-10 levels decrease significantly after VPA treatment, while IL-6 shows no significant change. (C) Seizure control time correlates with immunological parameters but not with VPA concentrations. (D) VPA concentrations in CSF are significantly lower than in plasma, with no change between d0 and d3, and no correlation with seizure control time. ∗∗∗P < 0.001, ∗∗P < 0.01, ∗P < 0.05; ns indicates not significant.

Article Snippet: Concentrations of IL-10 and IL-6 in plasma and CSF were quantified using commercial double-antibody sandwich ELISA kits (Boster Bioengineering, China), according to the manufacturer's instructions.

Techniques: Expressing, Concentration Assay, Clinical Proteomics, Control