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mog35  (Biosynth Carbosynth)


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    Structured Review

    Biosynth Carbosynth mog35
    Mog35, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 92/100, based on 72 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mog35/MOG(35-55)/bio_rxiv__64898__2026__01__08__698420-262-28-30
    Average 92 stars, based on 72 article reviews
    mog35 - by Bioz Stars, 2026-09
    92/100 stars

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    Injection:

    Article Title: Analysis of CNS autoimmunity in genetically diverse mice reveals unique phenotypes and mechanisms.
    Article Snippet: On D0 or D0 and D2, mice received 200 ng PTX (List Biological Laboratories) i.p. Mice were scored daily starting at D7 as described below. .. For MOG35–55 EAE, mice were injected s.c. with 200 μg MOG35–55 (New England Peptide) emulsified in CFA, supplemented with 4 mg/mL heat-killed M. tuberculosis, and were treated with a single i.p. injection of 200 ng PTX on D0. ..

    Article Title: Lactobacillus reuteri tryptophan metabolism promotes host susceptibility to CNS autoimmunity
    Article Snippet: .. Briefly, mice were injected subcutaneously on day 0 (lower flank) and day 7 (upper flank) with 50μl per flank of 0.1mg of myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) (New England Peptide, Inc. MA, USA) emulsified in PBS and 50% complete Freund’s adjuvant (CFA; Sigma, USA) supplemented with an additional 4 mg/ml Mycobacterium tuberculosis H37Ra (Difco, USA). ..

    Article Title: Integrated multi-omics analysis identifies microbial and metabolic signatures and drivers of CNS autoimmunity
    Article Snippet: EAE was induced using the 2×MOG35-55/CFA protocol in either exGF-B6 GMT recipients or C57BL/6J (Jackson Laboratory) [ ]. .. On day 0 (lower flank) and day 7 (upper flank) mice were injected subcutaneously with 50 μl per flank of 0.1 mg of myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) peptide (New England Peptide, Inc. MA, USA) emulsified in PBS and 50% complete Freund’s adjuvant (CFA; Sigma, USA) supplemented with an additional 4 mg/ml Mycobacterium tuberculosis H37Ra (Difco, USA). ..

    other:

    Article Title: Interleukin-17 affects synaptic plasticity and cognition in an experimental model of multiple sclerosis.
    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER CorelDRAW https://www.coreldraw.com/en/ 2021 ImageJ software National Institutes of Health, Bethesda, MD, USA https://rsb.info.nih.gov/ij/ iBright Imaging System Thermo Fisher Scientific CL750 Other Axoclamp amplifier Axon Instruments 2B Digidata Axon Instruments 1440A Microplate reader TECAN Infinite M200 Confocal mycroscopy ZEISS LSM 800 Differential interference contrast (Nomarski) and infrared microscopy Olympus BX51WI

    Article Title: Melatonin synergistically potentiates the effect of methylprednisolone on reducing neuroinflammation in the experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.
    Article Snippet: EAE was induced in the animals by subcutaneous immunization in both hind legs with 100 μg of MOG35–55 (Cambridge Research Biochemicals, Cleveland) emulsified in CFA (Sigma) containing 50 μg of heat-killed Mycobacterium tuberculosis (H37Ra, ATCC 25177) and two doses of intraperitoneal pertussis toxin (200 ng/day) (List Labs, California) on days 0 and 2 post-induction.

    Adjuvant:

    Article Title: A Lupin ( Lupinus angustifolius ) Protein Hydrolysate Decreases the Severity of Experimental Autoimmune Encephalomyelitis: A Preliminary Study.
    Article Snippet: .. Briefly, 100 μg of MOG35–55 peptide (Cambridge Research Biochemicals, Cambridge, UK) emulsified in complete Freud’s adjuvant (CFA, Sigma-Aldrich, St. Louis, MO, USA) containing 4 mg/mL of heat-inactivated Mycobacterium tuberculosis (Sigma-Aldrich) was inoculated subcutaneously. .. Furthermore, two doses of 400 ng pertussis toxin (Enzo Life Sciences, Farmingdale, NY, USA) were administered intraperitoneally on days 0 and 2 post-induction (p.i.) to induce the disease (Figure 6).

    Article Title: Lactobacillus reuteri tryptophan metabolism promotes host susceptibility to CNS autoimmunity
    Article Snippet: .. Briefly, mice were injected subcutaneously on day 0 (lower flank) and day 7 (upper flank) with 50μl per flank of 0.1mg of myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) (New England Peptide, Inc. MA, USA) emulsified in PBS and 50% complete Freund’s adjuvant (CFA; Sigma, USA) supplemented with an additional 4 mg/ml Mycobacterium tuberculosis H37Ra (Difco, USA). ..

    Article Title: Integrated multi-omics analysis identifies microbial and metabolic signatures and drivers of CNS autoimmunity
    Article Snippet: EAE was induced using the 2×MOG35-55/CFA protocol in either exGF-B6 GMT recipients or C57BL/6J (Jackson Laboratory) [ ]. .. On day 0 (lower flank) and day 7 (upper flank) mice were injected subcutaneously with 50 μl per flank of 0.1 mg of myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) peptide (New England Peptide, Inc. MA, USA) emulsified in PBS and 50% complete Freund’s adjuvant (CFA; Sigma, USA) supplemented with an additional 4 mg/ml Mycobacterium tuberculosis H37Ra (Difco, USA). ..



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    ZIKV infection exacerbates EAE. (a) Schematic illustration demonstrating the process of ZIKV infection and EAE induction by immunization with the <t>MOG35–55/CFA</t> emulsion in WT mice. (b and c) Clinical scores (b) and changes in body weight (c) in EAE ( n = 17) and ZIKV + EAE mice ( n = 16) over 21 days following immunization. Data were pooled from four independent experiments. (d and e) Representative hematoxylin and eosin (d) and Luxol fast blue staining (e) of spinal cord sections from CTRL, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. Arrows indicate lymphocyte infiltration in (d) and demyelination in (e). Scale bars, 100 μm. (f–h) RT-PCR analysis of Il17 (f), Ifng (g), and Csf2 (h) in the brain tissue of CTRL, ZIKV, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. The results were normalized to those of β-actin . CTRL, uninfected mice without EAE; ZIKV, ZIKV-infected mice without EAE. In d–h, data are represented as the mean ± SD of three independent experiments. Unpaired t -test; ***, P < 0.001; **, P < 0.01; *, P < 0.05.
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    RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of <t>MOG35-55-induced</t> EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control
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    RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of <t>MOG35-55-induced</t> EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control
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    RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of <t>MOG35-55-induced</t> EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control
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    Biosynth Carbosynth mog35
    RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of <t>MOG35-55-induced</t> EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control
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    Image Search Results


    ZIKV infection exacerbates EAE. (a) Schematic illustration demonstrating the process of ZIKV infection and EAE induction by immunization with the MOG35–55/CFA emulsion in WT mice. (b and c) Clinical scores (b) and changes in body weight (c) in EAE ( n = 17) and ZIKV + EAE mice ( n = 16) over 21 days following immunization. Data were pooled from four independent experiments. (d and e) Representative hematoxylin and eosin (d) and Luxol fast blue staining (e) of spinal cord sections from CTRL, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. Arrows indicate lymphocyte infiltration in (d) and demyelination in (e). Scale bars, 100 μm. (f–h) RT-PCR analysis of Il17 (f), Ifng (g), and Csf2 (h) in the brain tissue of CTRL, ZIKV, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. The results were normalized to those of β-actin . CTRL, uninfected mice without EAE; ZIKV, ZIKV-infected mice without EAE. In d–h, data are represented as the mean ± SD of three independent experiments. Unpaired t -test; ***, P < 0.001; **, P < 0.01; *, P < 0.05.

    Journal: International Immunology

    Article Title: Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes

    doi: 10.1093/intimm/dxaf075

    Figure Lengend Snippet: ZIKV infection exacerbates EAE. (a) Schematic illustration demonstrating the process of ZIKV infection and EAE induction by immunization with the MOG35–55/CFA emulsion in WT mice. (b and c) Clinical scores (b) and changes in body weight (c) in EAE ( n = 17) and ZIKV + EAE mice ( n = 16) over 21 days following immunization. Data were pooled from four independent experiments. (d and e) Representative hematoxylin and eosin (d) and Luxol fast blue staining (e) of spinal cord sections from CTRL, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. Arrows indicate lymphocyte infiltration in (d) and demyelination in (e). Scale bars, 100 μm. (f–h) RT-PCR analysis of Il17 (f), Ifng (g), and Csf2 (h) in the brain tissue of CTRL, ZIKV, EAE, and ZIKV + EAE mice obtained on Day 21 postimmunization. The results were normalized to those of β-actin . CTRL, uninfected mice without EAE; ZIKV, ZIKV-infected mice without EAE. In d–h, data are represented as the mean ± SD of three independent experiments. Unpaired t -test; ***, P < 0.001; **, P < 0.01; *, P < 0.05.

    Article Snippet: The MOG35–55 peptide (MEVGWYRSPFSRVVHLYRNGK) was synthesized by SynPeptide (Shanghai, China).

    Techniques: Infection, Emulsion, Staining, Reverse Transcription Polymerase Chain Reaction

    ZIKV infection potentiates T cell infiltration into the CNS in EAE. (a and b) Flow cytometric analysis of lymphocytes, representing the absolute number of CD4 + T cells in the brain (a) and spinal cord (b) per mouse, obtained on Day 21 postimmunization with MOG35–55/CFA emulsion in EAE, ZIKV + EAE, and CTRL mice. (c and d) Dot plots gated on CD4 + T cells stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies in the brain (c) and spinal cord (d). The numbers represent the percentage of cells in each quadrant. (e and f) Graphs represent the absolute numbers of Th17, Th1, and Th17.1 cells in the brain (e) and spinal cord (f) per mouse. CTRL, uninfected mice without EAE. In a–f, data are presented as the mean ± SD of three independent experiments. Unpaired t -test; **, P < 0.01; *, P < 0.05.

    Journal: International Immunology

    Article Title: Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes

    doi: 10.1093/intimm/dxaf075

    Figure Lengend Snippet: ZIKV infection potentiates T cell infiltration into the CNS in EAE. (a and b) Flow cytometric analysis of lymphocytes, representing the absolute number of CD4 + T cells in the brain (a) and spinal cord (b) per mouse, obtained on Day 21 postimmunization with MOG35–55/CFA emulsion in EAE, ZIKV + EAE, and CTRL mice. (c and d) Dot plots gated on CD4 + T cells stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies in the brain (c) and spinal cord (d). The numbers represent the percentage of cells in each quadrant. (e and f) Graphs represent the absolute numbers of Th17, Th1, and Th17.1 cells in the brain (e) and spinal cord (f) per mouse. CTRL, uninfected mice without EAE. In a–f, data are presented as the mean ± SD of three independent experiments. Unpaired t -test; **, P < 0.01; *, P < 0.05.

    Article Snippet: The MOG35–55 peptide (MEVGWYRSPFSRVVHLYRNGK) was synthesized by SynPeptide (Shanghai, China).

    Techniques: Infection, Emulsion, Staining

    Astrocyte-specific TRAF6-deficient mice are protected against ZIKV-induced exacerbation of EAE. (a) Clinical scores of WT EAE ( n = 14), WT ZIKV + EAE ( n = 14), TRAF6Δastro ( n = 14), and TRAF6Δastro ZIKV + EAE mice ( n = 15) over 21 days following immunization with MOG35–55/CFA emulsion. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections of mice treated as described in (a). Arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bar, 100 μm. (d) Flow cytometric analysis of lymphocytes representing the absolute number of CD4 + T cells in the brain of mice treated as in (a). Dot plots gated on CD4 + T cells stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies. The number represents the percentage of cells in each quadrant. (e) Graphs represent the absolute numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain. CTRL, uninfected mice without EAE. Data are pooled from two independent experiments in (a). Data are representative of two independent experiments in (b–e). Graphs represent mean ± SD. Unpaired t -test; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Journal: International Immunology

    Article Title: Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes

    doi: 10.1093/intimm/dxaf075

    Figure Lengend Snippet: Astrocyte-specific TRAF6-deficient mice are protected against ZIKV-induced exacerbation of EAE. (a) Clinical scores of WT EAE ( n = 14), WT ZIKV + EAE ( n = 14), TRAF6Δastro ( n = 14), and TRAF6Δastro ZIKV + EAE mice ( n = 15) over 21 days following immunization with MOG35–55/CFA emulsion. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections of mice treated as described in (a). Arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bar, 100 μm. (d) Flow cytometric analysis of lymphocytes representing the absolute number of CD4 + T cells in the brain of mice treated as in (a). Dot plots gated on CD4 + T cells stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies. The number represents the percentage of cells in each quadrant. (e) Graphs represent the absolute numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain. CTRL, uninfected mice without EAE. Data are pooled from two independent experiments in (a). Data are representative of two independent experiments in (b–e). Graphs represent mean ± SD. Unpaired t -test; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Article Snippet: The MOG35–55 peptide (MEVGWYRSPFSRVVHLYRNGK) was synthesized by SynPeptide (Shanghai, China).

    Techniques: Emulsion, Staining

    ZIKV-induced exacerbation of EAE is abolished in CCR2-deficient mice (a) clinical scores of uninfected WT ( n = 11), ZIKV-infected WT ( n = 11), uninfected CCR2-deficient ( n = 13), ZIKV-infected CCR2-deficient ( n = 13), uninfected CCR6-deficient ( n = 14), and ZIKV-infected CCR6-deficient mice ( n = 14) over 21 days following immunization with MOG35–55/CFA emulsion. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections from treated mice as described in (a). The arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bars, 100 μm. (d) Flow cytometric analysis of lymphocytes representing the absolute number of CD4 + T cells in the brain obtained on Day 21 postimmunization with the MOG35–55/CFA emulsion. CD4 + T cells were intracellularly stained with anti-IL-17 and anti-IFN-γ antibodies. The numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain are represented. Data were pooled from two independent experiments in (a). Data are representative of two independent experiments in (b–d). The graphs represent mean and SD values. Unpaired t -test; ***, P < 0.001; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Journal: International Immunology

    Article Title: Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes

    doi: 10.1093/intimm/dxaf075

    Figure Lengend Snippet: ZIKV-induced exacerbation of EAE is abolished in CCR2-deficient mice (a) clinical scores of uninfected WT ( n = 11), ZIKV-infected WT ( n = 11), uninfected CCR2-deficient ( n = 13), ZIKV-infected CCR2-deficient ( n = 13), uninfected CCR6-deficient ( n = 14), and ZIKV-infected CCR6-deficient mice ( n = 14) over 21 days following immunization with MOG35–55/CFA emulsion. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections from treated mice as described in (a). The arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bars, 100 μm. (d) Flow cytometric analysis of lymphocytes representing the absolute number of CD4 + T cells in the brain obtained on Day 21 postimmunization with the MOG35–55/CFA emulsion. CD4 + T cells were intracellularly stained with anti-IL-17 and anti-IFN-γ antibodies. The numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain are represented. Data were pooled from two independent experiments in (a). Data are representative of two independent experiments in (b–d). The graphs represent mean and SD values. Unpaired t -test; ***, P < 0.001; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Article Snippet: The MOG35–55 peptide (MEVGWYRSPFSRVVHLYRNGK) was synthesized by SynPeptide (Shanghai, China).

    Techniques: Infection, Emulsion, Staining

    Propagermanium efficiently suppresses the exacerbation of EAE by ZIKV infection. (a) Clinical scores of uninfected control ( n = 11), ZIKV-infected control ( n = 14), uninfected PG-administered ( n = 10), and ZIKV-infected PG-administered mice ( n = 11) over a period of 21 days following immunization with MOG35–55/CFA emulsion. Starting the day prior to MOG immunization, a daily oral dose of 5 mg/kg PG in 200 μl PBS was administered. The control group received 200 μl of PBS as the vehicle. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections from treated mice, as in (a). Arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bars, 100 μm. (d) Flow cytometric analysis of lymphocytes, representing the absolute number of CD4 + T cells in the brain of mice as treated in (a). CD4 + T cells were stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies. The numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain are shown. CTRL, uninfected mice with EAE. PG (+), PG-administered mice. Data were pooled from two independent experiments in (a) and two independent experiments in (b–d). The graphs represent mean and SD values. Unpaired t -test; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Journal: International Immunology

    Article Title: Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes

    doi: 10.1093/intimm/dxaf075

    Figure Lengend Snippet: Propagermanium efficiently suppresses the exacerbation of EAE by ZIKV infection. (a) Clinical scores of uninfected control ( n = 11), ZIKV-infected control ( n = 14), uninfected PG-administered ( n = 10), and ZIKV-infected PG-administered mice ( n = 11) over a period of 21 days following immunization with MOG35–55/CFA emulsion. Starting the day prior to MOG immunization, a daily oral dose of 5 mg/kg PG in 200 μl PBS was administered. The control group received 200 μl of PBS as the vehicle. (b and c) Representative hematoxylin and eosin (b) and Luxol fast blue staining (c) of spinal cord sections from treated mice, as in (a). Arrows indicate lymphocyte infiltration in (b) and demyelination in (c). Scale bars, 100 μm. (d) Flow cytometric analysis of lymphocytes, representing the absolute number of CD4 + T cells in the brain of mice as treated in (a). CD4 + T cells were stained intracellularly with anti-IL-17 and anti-IFN-γ antibodies. The numbers of CD4 + T, Th17, Th1, and Th17.1 cells in the brain are shown. CTRL, uninfected mice with EAE. PG (+), PG-administered mice. Data were pooled from two independent experiments in (a) and two independent experiments in (b–d). The graphs represent mean and SD values. Unpaired t -test; **, P < 0.01; *, P < 0.05; N.S., not significant.

    Article Snippet: The MOG35–55 peptide (MEVGWYRSPFSRVVHLYRNGK) was synthesized by SynPeptide (Shanghai, China).

    Techniques: Infection, Control, Emulsion, Staining

    RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of MOG35-55-induced EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control

    Journal: Journal of Neuroinflammation

    Article Title: TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination

    doi: 10.1186/s12974-026-03769-4

    Figure Lengend Snippet: RGMa is upregulated in MS patients and EAE mice and localizes to astrocytes. A RGMa levels in peripheral blood samples from MS patients (n = 117) and controls (n = 50), as quantified by ELISA. B Schematic depicting the time course of MOG35-55-induced EAE in the murine model. C Clinical scores of EAE mice following immunization with MOG35-55 peptide (n = 12). D Representative Western blot analysis of RGMa protein expression in brain lysates from EAE mice at 28 dpi (n = 5). E Corresponding Western blot analysis of RGMa expression in spinal cord lysates from EAE mice at 28 dpi (n = 5). F Quantitative assessment of RGMa protein expression in brain lysates, normalized to GAPDH (n = 5). G Quantification of RGMa expression in spinal cord lysates, normalized to GAPDH (n = 5). H Immunofluorescence analysis illustrating the spatial distribution and co-localization of RGMa (red) with the astrocyte marker glial fibrillary acidic protein (GFAP, green) in brain and lumbar spinal cord sections between control and EAE mice at 28 dpi (n = 5). Note: IgG isotype controls confirmed staining specificity (Fig. S2). Scale bar, 50 µm. DAPI, 4',6-Diamidino-2'-phenylindole. I Inflammatory cytokine mRNA expression levels of IL-1β, IL-6, and CCL2 in primary astrocytes at 24 hours after lentivirus-mediated overexpression of RGMa or vector control

    Article Snippet: After 10 days of induction with MOG35-55 by which time mice gradually exhibited tail weakness, the mice were randomly assigned to receive daily intraperitoneal injections of either Quisinostat (HY-12726, MedChemExpress, USA) at 10 mg/kg or an equal volume of vehicle control for 2 weeks.

    Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Marker, Control, Staining, Over Expression, Plasmid Preparation