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mouse monoclonal immunoglobulin ig g1 antibody (Hycult Biotech)

Name: mouse monoclonal immunoglobulin ig g1 antibody
Brand: Hycult Biotech
Rating: 92 (3 reviews)

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Hycult Biotech mouse monoclonal immunoglobulin ig g1 antibody
Mouse Monoclonal Immunoglobulin Ig G1 Antibody, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse monoclonal immunoglobulin ig g1 antibody/product/Hycult Biotech
Average 92 stars, based on 1 article reviews

mouse monoclonal immunoglobulin ig g1 antibody - by Bioz Stars, 2025-05

92/100 stars

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EAE was induced with MOG 35–55 in TNFR1 -/- , TNFR2 -/- and WT mice and the resulting disease was assessed daily using a score from 0 to 5, until 21 days after the onset of neurological symptoms. TNFR1 -/- mice had a much less severe disease course when compared to WT mice, whereas TNFR2 -/- mice showed more severe symptoms than WT mice ( A ). These observations were reflected in the significantly reduced cumulative EAE score in TNFR1 -/- mice, and the significantly increased cumulative score in TNFR2 -/- mice ( B ). Furthermore, TNFR1 -/- mice were more resistant to disease induction than both TNFR2 -/- and WT mice ( C ). * P<0.05, TNFR1 -/- n = 13; TNFR2 -/- n = 8; WT n = 14.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: EAE was induced with MOG 35–55 in TNFR1 -/- , TNFR2 -/- and WT mice and the resulting disease was assessed daily using a score from 0 to 5, until 21 days after the onset of neurological symptoms. TNFR1 -/- mice had a much less severe disease course when compared to WT mice, whereas TNFR2 -/- mice showed more severe symptoms than WT mice ( A ). These observations were reflected in the significantly reduced cumulative EAE score in TNFR1 -/- mice, and the significantly increased cumulative score in TNFR2 -/- mice ( B ). Furthermore, TNFR1 -/- mice were more resistant to disease induction than both TNFR2 -/- and WT mice ( C ). * P<0.05, TNFR1 -/- n = 13; TNFR2 -/- n = 8; WT n = 14.

Article Snippet: Mice were injected i.p. with either anti-mouse TNFR1 (HM1097, Hycult Biotech, Uden, The Netherlands) or an isotype control antibody (Armenian Hamster IgG negative control, AbD Serotec, Düsseldorf, Germany) diluted in saline.

Techniques:

Spinal cords were analysed at day 21 of EAE for signs of inflammatory infiltration, demyelination and axonal degeneration. TNFR1 -/- mice had significantly less infiltration of both CD3-positive T cells ( A ) and Mac-3-positive activated microglia/macrophages ( B ) when compared to WT and TNFR2 -/- mice. Furthermore, TNFR1 -/- mice also had significantly less demyelination, as assessed by LFB staining ( C ) and axonal damage, as assessed by accumulation of β-APP-positive axonal profiles ( D ), when compared to both WT and TNFR2 -/- mice. Conversely, TNFR2 -/- had significantly increased numbers of β-APP positive damaged axons compared to WT mice.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: Spinal cords were analysed at day 21 of EAE for signs of inflammatory infiltration, demyelination and axonal degeneration. TNFR1 -/- mice had significantly less infiltration of both CD3-positive T cells ( A ) and Mac-3-positive activated microglia/macrophages ( B ) when compared to WT and TNFR2 -/- mice. Furthermore, TNFR1 -/- mice also had significantly less demyelination, as assessed by LFB staining ( C ) and axonal damage, as assessed by accumulation of β-APP-positive axonal profiles ( D ), when compared to both WT and TNFR2 -/- mice. Conversely, TNFR2 -/- had significantly increased numbers of β-APP positive damaged axons compared to WT mice.

Techniques: Staining

L929 cells were incubated with recombinant mouse TNF in the presence or absence of 10 µg/ml anti-TNFR1 ( A ) or with anti-TNFR1 in the presence of 0.1 ng/ml mouse TNF ( B ) and cell survival was determined by crystal violet staining. C, D : Female C57BL/6 wild type mice were pretreated with PBS or anti-TNFR1 (10 mg/kg, i.p.). After 2 h, PBS or murine TNF were injected i.v. (1 mg/kg) and body temperature ( C ) as well as survival of animals ( D ) were determined.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: L929 cells were incubated with recombinant mouse TNF in the presence or absence of 10 µg/ml anti-TNFR1 ( A ) or with anti-TNFR1 in the presence of 0.1 ng/ml mouse TNF ( B ) and cell survival was determined by crystal violet staining. C, D : Female C57BL/6 wild type mice were pretreated with PBS or anti-TNFR1 (10 mg/kg, i.p.). After 2 h, PBS or murine TNF were injected i.v. (1 mg/kg) and body temperature ( C ) as well as survival of animals ( D ) were determined.

Techniques: Incubation, Recombinant, Staining, Injection

Anti-mouse TNFR1 was injected intra-peritoneally in C57BL/6 mice, on the day of disease induction, at a dosage of 100 µg (equivalent to 5 mg/kg). Mice were subsequently monitored on a daily basis until 21 days after the onset of clinical symptoms (EAE day 21). Antibody treatment resulted in a reduced EAE severity compared to mice receiving control IgG ( A, B ). Furthermore, mice injected with anti-TNFR1 also showed a significant delay in the onset of spinal cord symptoms in comparison to mice receiving control IgG ( C ). (A) Results from one representative experiment out of four shown (control IgG n = 4; anti TNFR1 n = 6), (B, C) results from four combined experiments (control IgG n = 16, anti-TNFR1 n = 19). * P<0.05, **P<0.01.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: Anti-mouse TNFR1 was injected intra-peritoneally in C57BL/6 mice, on the day of disease induction, at a dosage of 100 µg (equivalent to 5 mg/kg). Mice were subsequently monitored on a daily basis until 21 days after the onset of clinical symptoms (EAE day 21). Antibody treatment resulted in a reduced EAE severity compared to mice receiving control IgG ( A, B ). Furthermore, mice injected with anti-TNFR1 also showed a significant delay in the onset of spinal cord symptoms in comparison to mice receiving control IgG ( C ). (A) Results from one representative experiment out of four shown (control IgG n = 4; anti TNFR1 n = 6), (B, C) results from four combined experiments (control IgG n = 16, anti-TNFR1 n = 19). * P<0.05, **P<0.01.

Techniques: Injection

Characteristics of EAE following anti-TNFR1 treatment from the day of immunization.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: Characteristics of EAE following anti-TNFR1 treatment from the day of immunization.

Techniques:

Spinal cord histopathology was performed at day 21 of EAE, following treatment with anti-mouse TNFR1 on the day of immunization. Representative images are shown from control IgG treated mice, with an EAE score of 2.0 ( B, E, H , and K ) and from anti-TNFR1-treated animals, with an EAE score of 1.0 ( C, F, I and L ). The level of spinal cord demyelination was assessed using sections stained with LFB ( A–C ). Mice treated prophylactically with anti-TNFR1 had significantly reduced levels of demyelination compared to control-treated mice ( A–C ). Immunohistochemistry with an anti-CD3 antibody was used to detect T cells and showed a decrease, although not significant, in the number of T cells within the spinal cord of anti-TNFR1 treated mice, in comparison to control animals ( D–F ). Immunohistochemistry with an antibody to Mac-3 was used to detect activated microglia and macrophages and demonstrated a decrease in the number of positive cells in anti-TNFR1 treated mice, although again this was not significant ( G–I ). J-L : Immunohistochemistry with an anti-NeuN antibody was used to detect neuronal cell bodies, which were quantified within the spinal cord grey matter. Anti-TNFR1 treated mice had significantly elevated numbers of surviving neuronal cell bodies. Scale bars in B, C, E, F, H, I, K, L : 200 µm.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: Spinal cord histopathology was performed at day 21 of EAE, following treatment with anti-mouse TNFR1 on the day of immunization. Representative images are shown from control IgG treated mice, with an EAE score of 2.0 ( B, E, H , and K ) and from anti-TNFR1-treated animals, with an EAE score of 1.0 ( C, F, I and L ). The level of spinal cord demyelination was assessed using sections stained with LFB ( A–C ). Mice treated prophylactically with anti-TNFR1 had significantly reduced levels of demyelination compared to control-treated mice ( A–C ). Immunohistochemistry with an anti-CD3 antibody was used to detect T cells and showed a decrease, although not significant, in the number of T cells within the spinal cord of anti-TNFR1 treated mice, in comparison to control animals ( D–F ). Immunohistochemistry with an antibody to Mac-3 was used to detect activated microglia and macrophages and demonstrated a decrease in the number of positive cells in anti-TNFR1 treated mice, although again this was not significant ( G–I ). J-L : Immunohistochemistry with an anti-NeuN antibody was used to detect neuronal cell bodies, which were quantified within the spinal cord grey matter. Anti-TNFR1 treated mice had significantly elevated numbers of surviving neuronal cell bodies. Scale bars in B, C, E, F, H, I, K, L : 200 µm.

Techniques: Histopathology, Staining, Immunohistochemistry

EAE was induced in C57BL/6 mice with MOG 35–55 and mice were assessed for neurological symptoms on a daily basis. 400 µg (equivalent to 20 mg/kg) anti-mouse TNFR1 was injected i.p. either once on the day of EAE onset, or twice; firstly on the day of EAE onset and again on day 4 of the disease. Control mice received two injections of control IgG on days 1 and 4 of EAE. Mice receiving two injections of anti-TNFR1 had significantly reduced neurological symptoms than mice receiving control IgG ( A , B ). Spinal cords were examined histopathologically at day 14 of EAE by LFB staining ( C – E ). Control IgG-treated mice ( D , image from animal with an EAE score of 2.5) had more demyelination than mice treated with two injections of anti-TNFR1 ( E , image from animal with an EAE score of 0.5), although this was not found to be statistically significant. Immunohistochemistry with an anti-CD3 antibody showed no difference in the number of T cells within the spinal cord of control IgG-treated animals ( F , G , image from an animal with an EAE score of 2.5) and anti-TNFR1 treated mice ( H , image from an animal with an EAE score of 2.0). Immunohistochemistry with an antibody to Mac-3 also demonstrated no difference in the number of activated microglia/macrophages within the spinal cord of control IgG-treated animals ( I , J , image from an animal with an EAE score of 2.5) and anti-TNFR1 treated mice ( K , image from an animal with an EAE score of 2.0). L – N : Immunohistochemistry with an antibody against NeuN showed a statistically non-significant trend towards neuroprotection in the anti-TNFR1-treated mice ( M , image from a control IgG-treated animal with an EAE score of 1.5), ( N , image from an anti-TNFR1-treated animal with an EAE score of 1.5). Scale bars in D , E, G, H, J, K, M, N : 200 µm. * P<0.05. Control IgG n = 9; anti-TNFR1: 1 injection n = 4; anti-TNFR1: 2 injections n = 8.

Journal: PLoS ONE

Article Title: Antibody-Mediated Inhibition of TNFR1 Attenuates Disease in a Mouse Model of Multiple Sclerosis

doi: 10.1371/journal.pone.0090117

Figure Lengend Snippet: EAE was induced in C57BL/6 mice with MOG 35–55 and mice were assessed for neurological symptoms on a daily basis. 400 µg (equivalent to 20 mg/kg) anti-mouse TNFR1 was injected i.p. either once on the day of EAE onset, or twice; firstly on the day of EAE onset and again on day 4 of the disease. Control mice received two injections of control IgG on days 1 and 4 of EAE. Mice receiving two injections of anti-TNFR1 had significantly reduced neurological symptoms than mice receiving control IgG ( A , B ). Spinal cords were examined histopathologically at day 14 of EAE by LFB staining ( C – E ). Control IgG-treated mice ( D , image from animal with an EAE score of 2.5) had more demyelination than mice treated with two injections of anti-TNFR1 ( E , image from animal with an EAE score of 0.5), although this was not found to be statistically significant. Immunohistochemistry with an anti-CD3 antibody showed no difference in the number of T cells within the spinal cord of control IgG-treated animals ( F , G , image from an animal with an EAE score of 2.5) and anti-TNFR1 treated mice ( H , image from an animal with an EAE score of 2.0). Immunohistochemistry with an antibody to Mac-3 also demonstrated no difference in the number of activated microglia/macrophages within the spinal cord of control IgG-treated animals ( I , J , image from an animal with an EAE score of 2.5) and anti-TNFR1 treated mice ( K , image from an animal with an EAE score of 2.0). L – N : Immunohistochemistry with an antibody against NeuN showed a statistically non-significant trend towards neuroprotection in the anti-TNFR1-treated mice ( M , image from a control IgG-treated animal with an EAE score of 1.5), ( N , image from an anti-TNFR1-treated animal with an EAE score of 1.5). Scale bars in D , E, G, H, J, K, M, N : 200 µm. * P<0.05. Control IgG n = 9; anti-TNFR1: 1 injection n = 4; anti-TNFR1: 2 injections n = 8.

Techniques: Injection, Staining, Immunohistochemistry

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