trail-neutralizing antibodies clone n2b2 Search Results


anti trail monoclonal antibody  (Bio X Cell)
98
Bio X Cell anti trail monoclonal antibody
Figure 7 Pulmonary inflammation is suppressed and emphysema-like alveolar enlargement inhibited in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand <t>(TRAIL).</t> Wild-type mice were exposed to cigarette smoke or normal air for twelve weeks and treated with neutralizing anti-TRAIL <t>monoclonal</t> antibody or isotype control, intraperitoneally three times per week, from week 7 to 12. (a) Total leukocytes, (b) macrophages, (c) neutrophils, and (d) lymphocytes were enumerated in May-Grunwald Giemsa-stained bronchoalveolar lavage (BAL). (e) The numbers of parenchymal inflammatory cells (arrowheads) were determined in periodic acid- Schiff-stained lung sections. (f) NF-kB p65 activity in whole-lung homogenates. (g) Alveolar diameter (mm) was determined in hematoxylin and eosin- stained lung sections using the mean linear intercept technique. (h) The numbers of TUNEL þ (terminal deoxynucleotidyl transferase dUTP nick end labeling) cells (arrowheads) enumerated in whole-lung sections. Data (n ¼ 5–6) presented as means±s.e.m. are representative of two independent experiments. **Po0.01; ***Po0.001; ****Po0.0001 compared with isotype-treated or anti-TRAIL-treated normal air-exposed controls. #Po0.05; ##Po0.01; ###Po0.001; ####Po0.0001 compared with isotype-treated CS-exposed controls.
Anti Trail Monoclonal Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/trail-neutralizing+antibodies+clone+n2b2/pm26555706-199-12-24?v=Bio+X+Cell
Average 98 stars, based on 1 article reviews
anti trail monoclonal antibody - by Bioz Stars, 2026-08
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Figure 7 Pulmonary inflammation is suppressed and emphysema-like alveolar enlargement inhibited in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Wild-type mice were exposed to cigarette smoke or normal air for twelve weeks and treated with neutralizing anti-TRAIL monoclonal antibody or isotype control, intraperitoneally three times per week, from week 7 to 12. (a) Total leukocytes, (b) macrophages, (c) neutrophils, and (d) lymphocytes were enumerated in May-Grunwald Giemsa-stained bronchoalveolar lavage (BAL). (e) The numbers of parenchymal inflammatory cells (arrowheads) were determined in periodic acid- Schiff-stained lung sections. (f) NF-kB p65 activity in whole-lung homogenates. (g) Alveolar diameter (mm) was determined in hematoxylin and eosin- stained lung sections using the mean linear intercept technique. (h) The numbers of TUNEL þ (terminal deoxynucleotidyl transferase dUTP nick end labeling) cells (arrowheads) enumerated in whole-lung sections. Data (n ¼ 5–6) presented as means±s.e.m. are representative of two independent experiments. **Po0.01; ***Po0.001; ****Po0.0001 compared with isotype-treated or anti-TRAIL-treated normal air-exposed controls. #Po0.05; ##Po0.01; ###Po0.001; ####Po0.0001 compared with isotype-treated CS-exposed controls.

Journal: Mucosal immunology

Article Title: A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.

doi: 10.1038/mi.2015.111

Figure Lengend Snippet: Figure 7 Pulmonary inflammation is suppressed and emphysema-like alveolar enlargement inhibited in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Wild-type mice were exposed to cigarette smoke or normal air for twelve weeks and treated with neutralizing anti-TRAIL monoclonal antibody or isotype control, intraperitoneally three times per week, from week 7 to 12. (a) Total leukocytes, (b) macrophages, (c) neutrophils, and (d) lymphocytes were enumerated in May-Grunwald Giemsa-stained bronchoalveolar lavage (BAL). (e) The numbers of parenchymal inflammatory cells (arrowheads) were determined in periodic acid- Schiff-stained lung sections. (f) NF-kB p65 activity in whole-lung homogenates. (g) Alveolar diameter (mm) was determined in hematoxylin and eosin- stained lung sections using the mean linear intercept technique. (h) The numbers of TUNEL þ (terminal deoxynucleotidyl transferase dUTP nick end labeling) cells (arrowheads) enumerated in whole-lung sections. Data (n ¼ 5–6) presented as means±s.e.m. are representative of two independent experiments. **Po0.01; ***Po0.001; ****Po0.0001 compared with isotype-treated or anti-TRAIL-treated normal air-exposed controls. #Po0.05; ##Po0.01; ###Po0.001; ####Po0.0001 compared with isotype-treated CS-exposed controls.

Article Snippet: Mice were treated with 12.5 mg kg 1 body weight of neutralizing anti-TRAIL monoclonal antibody (clone N2B2) or rat IgG2a isotype control (clone 2A3, BioXCell, West Lebanon, NH) from week 7 to 12 (six weeks), by intraperitoneally injections three times per week.6 Statistical analysis.

Techniques: Neutralization, Control, Staining, Activity Assay, TUNEL Assay

Figure 8 Airway remodeling is reduced in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Wild-type mice were exposed to cigarette smoke (CS) or normal air for twelve weeks and treated with neutralizing anti-TRAIL monoclonal or isotype control antibodies, intraperitoneally three times per week, from weeks 7 to 12. (a) Small airway epithelial thickness in terms of epithelial cell area (mm2) per basement membrane (BM) perimeter (mm) was determined in periodic acid-Schiff (PAS)-stained lung sections. (b) The number of epithelial cells in PAS-stained lung sections was assessed by enumerating the number of nuclei per 100 mm BM perimeter. (c) Area of collagen deposition (mm2) per BM perimeter (mm) in Masson’s Trichrome-stained lung sections. Data (n ¼ 5–6) presented as means±s.e.m. are representative of two independent experiments. **Po0.01; ****Po0.0001 compared with anti-TRAIL or isotype normal air-exposed controls. #Po0.05; ###Po0.001 compared with isotype-treated CS-exposed controls.

Journal: Mucosal immunology

Article Title: A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.

doi: 10.1038/mi.2015.111

Figure Lengend Snippet: Figure 8 Airway remodeling is reduced in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Wild-type mice were exposed to cigarette smoke (CS) or normal air for twelve weeks and treated with neutralizing anti-TRAIL monoclonal or isotype control antibodies, intraperitoneally three times per week, from weeks 7 to 12. (a) Small airway epithelial thickness in terms of epithelial cell area (mm2) per basement membrane (BM) perimeter (mm) was determined in periodic acid-Schiff (PAS)-stained lung sections. (b) The number of epithelial cells in PAS-stained lung sections was assessed by enumerating the number of nuclei per 100 mm BM perimeter. (c) Area of collagen deposition (mm2) per BM perimeter (mm) in Masson’s Trichrome-stained lung sections. Data (n ¼ 5–6) presented as means±s.e.m. are representative of two independent experiments. **Po0.01; ****Po0.0001 compared with anti-TRAIL or isotype normal air-exposed controls. #Po0.05; ###Po0.001 compared with isotype-treated CS-exposed controls.

Article Snippet: Mice were treated with 12.5 mg kg 1 body weight of neutralizing anti-TRAIL monoclonal antibody (clone N2B2) or rat IgG2a isotype control (clone 2A3, BioXCell, West Lebanon, NH) from week 7 to 12 (six weeks), by intraperitoneally injections three times per week.6 Statistical analysis.

Techniques: Neutralization, Control, Membrane, Staining