tnf α neutralizing antibody infliximab Search Results


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Janssen anti tnfα monoclonal antibody

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Schering-Plough corporation tnfα blockers
<t>Infliximab</t> enhances plasma cell differentiation. (a) Circulating plasma cell levels in rheumatoid arthritis (RA) patients treated by infliximab with anti-nuclear antibody (ANA) (n = 10) or without ANA production (n = 10), in patients with active systemic lupus erythematosus (SLE) (n = 10), and in healthy volunteers (n = 10). Plasma cell levels were measured in peripheral blood. The mean number/milliliter of CD38 + CD19 + CD20 - is shown (mean ± standard deviation). * P < 0.001, Mann–Whitney U test. (b) Peripheral blood mononuclear cells (PBMCs) from healthy donors were cultured out in the presence of influenza virus (Flu) with or without infliximab or <t>TNFα.</t> After 10 days, we analyzed by flow cytometry the proportion of CD19 + CD20 - CD38 high+ plasma cells. Data expressed as the mean ± standard error of the mean of three independent experiments. (c) PBMCs from healthy donors, from RA patients treated by infliximab and developing ANAs, and from SLE patients were cultured in the presence of influenza virus with or without the TNFα blocker, infliximab. After 15 days, ANA titers were measured in the supernatants. Data expressed as mean ± standard error of the mean of three independent experiments.
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MedChemExpress tnf α specific inhibitor
Cell-to-cell communication analysis revealing stromal cells differentiate towards ossification by interacting with immune cells. (A) Cellphone DB analysis showing many interactions between immune cells and stromal cells 3, 4, 5. (B) Human degenerative NP cells were treated <t>with</t> <t>TNF-α</t> for 24 hours to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (C) Human degenerative NP cells were treated with CD74 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (D) Human degenerative NP cells were treated with CCL-3 and CCL-2 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 250 μm. n=5, * vs control, p<0.05. (E) Human degenerative NP cells were treated with TNF-α and MAPK inhibitor (U0126) to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. ** p<0.01; *** p<0.001.
Tnf α Specific Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Journal: iScience

Article Title: TRAIL-dependent apoptosis of peritoneal mesothelial cells by NK cells promotes ovarian cancer invasion

doi: 10.1016/j.isci.2023.108401

Figure Lengend Snippet:

Article Snippet: Chimeric human-murin anti-human-TNFα (Infliximab, Remsima) , Celltrion Healthcare , kind gift from Christian Bauer, Clinic for Gastroenterology, Endocrinology, Infectiology and Metabolism, Philipps University Marburg, Germany.

Techniques: Control, Recombinant, Polymer, Software

Infliximab enhances plasma cell differentiation. (a) Circulating plasma cell levels in rheumatoid arthritis (RA) patients treated by infliximab with anti-nuclear antibody (ANA) (n = 10) or without ANA production (n = 10), in patients with active systemic lupus erythematosus (SLE) (n = 10), and in healthy volunteers (n = 10). Plasma cell levels were measured in peripheral blood. The mean number/milliliter of CD38 + CD19 + CD20 - is shown (mean ± standard deviation). * P < 0.001, Mann–Whitney U test. (b) Peripheral blood mononuclear cells (PBMCs) from healthy donors were cultured out in the presence of influenza virus (Flu) with or without infliximab or TNFα. After 10 days, we analyzed by flow cytometry the proportion of CD19 + CD20 - CD38 high+ plasma cells. Data expressed as the mean ± standard error of the mean of three independent experiments. (c) PBMCs from healthy donors, from RA patients treated by infliximab and developing ANAs, and from SLE patients were cultured in the presence of influenza virus with or without the TNFα blocker, infliximab. After 15 days, ANA titers were measured in the supernatants. Data expressed as mean ± standard error of the mean of three independent experiments.

Journal: Arthritis Research & Therapy

Article Title: Myeloid dendritic cells correlate with clinical response whereas plasmacytoid dendritic cells impact autoantibody development in rheumatoid arthritis patients treated with infliximab

doi: 10.1186/ar2746

Figure Lengend Snippet: Infliximab enhances plasma cell differentiation. (a) Circulating plasma cell levels in rheumatoid arthritis (RA) patients treated by infliximab with anti-nuclear antibody (ANA) (n = 10) or without ANA production (n = 10), in patients with active systemic lupus erythematosus (SLE) (n = 10), and in healthy volunteers (n = 10). Plasma cell levels were measured in peripheral blood. The mean number/milliliter of CD38 + CD19 + CD20 - is shown (mean ± standard deviation). * P < 0.001, Mann–Whitney U test. (b) Peripheral blood mononuclear cells (PBMCs) from healthy donors were cultured out in the presence of influenza virus (Flu) with or without infliximab or TNFα. After 10 days, we analyzed by flow cytometry the proportion of CD19 + CD20 - CD38 high+ plasma cells. Data expressed as the mean ± standard error of the mean of three independent experiments. (c) PBMCs from healthy donors, from RA patients treated by infliximab and developing ANAs, and from SLE patients were cultured in the presence of influenza virus with or without the TNFα blocker, infliximab. After 15 days, ANA titers were measured in the supernatants. Data expressed as mean ± standard error of the mean of three independent experiments.

Article Snippet: PBMCs (1 × 10 6 /well) were then cultured with 10 4 influenza virus particles (Charles Rivers, Wilmington, MA, USA) with or without TNFα (10 μg/ml; R&D Systems) or TNFα blockers (Infliximab 20 μg/ml; Schering-Plough, Levallois-Perret, France) in a 48-well plate in 10% FCS RPMI supplemented with rhIL-2 (50 U/ml; R&D Systems, Lille, France).

Techniques: Cell Differentiation, Standard Deviation, MANN-WHITNEY, Cell Culture, Flow Cytometry

Cell-to-cell communication analysis revealing stromal cells differentiate towards ossification by interacting with immune cells. (A) Cellphone DB analysis showing many interactions between immune cells and stromal cells 3, 4, 5. (B) Human degenerative NP cells were treated with TNF-α for 24 hours to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (C) Human degenerative NP cells were treated with CD74 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (D) Human degenerative NP cells were treated with CCL-3 and CCL-2 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 250 μm. n=5, * vs control, p<0.05. (E) Human degenerative NP cells were treated with TNF-α and MAPK inhibitor (U0126) to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. ** p<0.01; *** p<0.001.

Journal: Frontiers in Immunology

Article Title: Single-cell RNA-seq analysis reveals that immune cells induce human nucleus pulposus ossification and degeneration

doi: 10.3389/fimmu.2023.1224627

Figure Lengend Snippet: Cell-to-cell communication analysis revealing stromal cells differentiate towards ossification by interacting with immune cells. (A) Cellphone DB analysis showing many interactions between immune cells and stromal cells 3, 4, 5. (B) Human degenerative NP cells were treated with TNF-α for 24 hours to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (C) Human degenerative NP cells were treated with CD74 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. (D) Human degenerative NP cells were treated with CCL-3 and CCL-2 to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 250 μm. n=5, * vs control, p<0.05. (E) Human degenerative NP cells were treated with TNF-α and MAPK inhibitor (U0126) to explore the expression of ossification markers (COL1A1 and RUNX2) by immunofluorescence staining. PBS was used as a negative control. Scale bar, 500 μm. n=5, * vs control, p<0.05. ** p<0.01; *** p<0.001.

Article Snippet: For twelve rats, the TNF-α specific inhibitor (MedChemExpress, Infliximab: HY-P9970) were injected during the puncture process.

Techniques: Expressing, Immunofluorescence, Staining, Negative Control, Control

Inhibition of TNF-α in the established rat disc degeneration model. (A) The expression of TNF-α in the established rat disc degeneration model. (B) The expression of ossification markers (COL1A1 and RUNX2) after inhibiting the role of TNF-α by administration of infliximab. (C) HE staining of intervertebral disc after inhibiting the role of TNF-α by administration of infliximab. (D) Safranin O-fast green staining of intervertebral disc after inhibiting the role of TNF-α by administration of infliximab. (E) X rays of rat coccyx disc after inhibiting the role of TNF-α by administration of infliximab. (F) MRI imaging of rat coccyx disc after inhibiting the role of TNF-α by administration of infliximab. AFP, annulus fibrous puncture. *p<0.05.

Journal: Frontiers in Immunology

Article Title: Single-cell RNA-seq analysis reveals that immune cells induce human nucleus pulposus ossification and degeneration

doi: 10.3389/fimmu.2023.1224627

Figure Lengend Snippet: Inhibition of TNF-α in the established rat disc degeneration model. (A) The expression of TNF-α in the established rat disc degeneration model. (B) The expression of ossification markers (COL1A1 and RUNX2) after inhibiting the role of TNF-α by administration of infliximab. (C) HE staining of intervertebral disc after inhibiting the role of TNF-α by administration of infliximab. (D) Safranin O-fast green staining of intervertebral disc after inhibiting the role of TNF-α by administration of infliximab. (E) X rays of rat coccyx disc after inhibiting the role of TNF-α by administration of infliximab. (F) MRI imaging of rat coccyx disc after inhibiting the role of TNF-α by administration of infliximab. AFP, annulus fibrous puncture. *p<0.05.

Article Snippet: For twelve rats, the TNF-α specific inhibitor (MedChemExpress, Infliximab: HY-P9970) were injected during the puncture process.

Techniques: Inhibition, Expressing, Staining, Imaging