Mouse CXCL10/IP-10/CRG-2 Antibody

Chemotaxis Induced by CXCL10/CRG‑2 and Neutralization by Mouse CXCL10/CRG‑2 Antibody. Recombinant Mouse CXCL10/CRG‑2 (Catalog # 466-CR) chemoattracts the BaF3 mouse pro‑B cell line transfected with human CXCR3 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (Catalog # AR002). Chemotaxis elicited by Recombinant Mouse CXCL10/CRG‑2 (0.5 µg/mL) is neutralized (green line) by increasing concentrations of Mouse CXCL10/CRG‑2 Monoclonal Antibody (Catalog # MAB466). The ND₅₀ is typically 10-40 µg/mL.

Detection of Mouse CXCL10/IP-10/CRG-2 by Immunohistochemistry Anti-CXCL10 treatment in atherosclerosis susceptible mice results in a change into a more stable lesion phenotype. A flow-altering device around the common carotid artery induced atherosclerosis in ApoE−/− mice. From week 1 to 4 of lesion development, a bioactivity-neutralizing anti-CXCL10 antibody was injected. After 9 weeks, lesions were compared to untreated controls by histology. The pictures show representative histological sections of treated and control mice. All photographs have been made with the same magnification (100x). Scale bars are provided in (e) and represent 100 μm. Data in bar diagrams are the mean values ± SD of at least 8 sections from at least 10 different animals per group. CXCL10 inhibition resulted in a more stable morphology evidenced by unchanged amounts of lesion macrophages (a), increased amounts of collagen (b), decreased macrophage activation (c), increased numbers of SMC (d), and reduced necrotic core size (e). *P < 0.05, **P < 0.01. MHC-II: Major Histocompatibility Complex Class II, SMC: smooth muscle cell. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/22164344), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CXCL10/IP-10/CRG-2 by Immunohistochemistry Anti-CXCL10 treatment in atherosclerosis susceptible mice results in a change into a more stable lesion phenotype. A flow-altering device around the common carotid artery induced atherosclerosis in ApoE−/− mice. From week 1 to 4 of lesion development, a bioactivity-neutralizing anti-CXCL10 antibody was injected. After 9 weeks, lesions were compared to untreated controls by histology. The pictures show representative histological sections of treated and control mice. All photographs have been made with the same magnification (100x). Scale bars are provided in (e) and represent 100 μm. Data in bar diagrams are the mean values ± SD of at least 8 sections from at least 10 different animals per group. CXCL10 inhibition resulted in a more stable morphology evidenced by unchanged amounts of lesion macrophages (a), increased amounts of collagen (b), decreased macrophage activation (c), increased numbers of SMC (d), and reduced necrotic core size (e). *P < 0.05, **P < 0.01. MHC-II: Major Histocompatibility Complex Class II, SMC: smooth muscle cell. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/22164344), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse CXCL10/IP-10/CRG-2 by Immunohistochemistry Anti-CXCL10 treatment in atherosclerosis susceptible mice results in a change into a more stable lesion phenotype. A flow-altering device around the common carotid artery induced atherosclerosis in ApoE−/− mice. From week 1 to 4 of lesion development, a bioactivity-neutralizing anti-CXCL10 antibody was injected. After 9 weeks, lesions were compared to untreated controls by histology. The pictures show representative histological sections of treated and control mice. All photographs have been made with the same magnification (100x). Scale bars are provided in (e) and represent 100 μm. Data in bar diagrams are the mean values ± SD of at least 8 sections from at least 10 different animals per group. CXCL10 inhibition resulted in a more stable morphology evidenced by unchanged amounts of lesion macrophages (a), increased amounts of collagen (b), decreased macrophage activation (c), increased numbers of SMC (d), and reduced necrotic core size (e). *P < 0.05, **P < 0.01. MHC-II: Major Histocompatibility Complex Class II, SMC: smooth muscle cell. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/22164344), licensed under a CC-BY license. Not internally tested by R&D Systems.