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R&D Systems goat anti cxcl9
Goat Anti Cxcl9, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 75 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/goat+anti+mouse+cxcl9/Mouse+CXCL9%2FMIG+Antibody/bio_rxiv__2025__03__18__643566-54-27-30
Average 94 stars, based on 75 article reviews

goat anti cxcl9 - by Bioz Stars, 2026-09

94/100 stars

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Article Title: A THERAPEUTIC OX40 AGONIST DYNAMICALLY ALTERS DENDRITIC, ENDOTHELIAL AND T CELL SUBSETS WITHIN THE ESTABLISHED TUMOR MICROENVIRONMENT
Article Snippet: .. The following primary antibodies were used for staining sections: rat anti-mouse CD31 (BD Biosciences), goat anti-mouse OX40 (Santa Cruz Biotechnology), rat anti-mouse OX40 (eBioscience), hamster anti-mouse CD11c (BD Biosciences), rat anti-mouse VCAM-1 (Santa Cruz Biotechnology), and goat anti-mouse CXCL9 (R&D Systems). .. The following secondary antibodies were used: donkey anti-rat Alexa Fluor 488 (Molecular Probes), donkey anti-goat Cy3 (Jackson ImmunoResearch), donkey anti-hamster Alexa Fluor 488 (Molecular Probes), donkey anti-rat Cy3 (Jackson ImmunoResearch), goat anti-rat Fab1 fragment Cy3 (Jackson ImmunoResearch), and goat anti-rat Alexa Fluor 488 (Molecular Probes).

Article Title: Astrocyte-Derived CXCL10 Drives Accumulation of Antibody-Secreting Cells in the Central Nervous System during Viral Encephalomyelitis
Article Snippet: .. For detection of CXCL9 and CXCL10, longitudinal sections were fixed with 4% paraformaldehyde for 20 min, treated with 1% Triton X-100 in PBS at room temperature, blocked for 30 min, and then stained with rabbit anti-mouse laminin (Cedarlane Laboratories, Ontario, Canada), rat anti-mouse CD138 (BD Bioscience), goat anti-mouse CXCL9 (AF-492-NA; R&D Systems), goat anti-mouse CXCL10 (AF-466-NA; R&D Systems), rat anti-mouse glial fibrillary acidic protein (GFAP) (2.2B10; Invitrogen), rabbit anti-mouse ionized calcium binding adaptor molecule-1 (Iba-1) (Wako, Richmond, VA), anti-mouse CD31 (550274; BD Bioscience), or anti-JHMV monoclonal Ab overnight at 4°C. ..

Article Title: Astrocyte-Derived CXCL10 Drives Accumulation of Antibody-Secreting Cells in the Central Nervous System during Viral Encephalomyelitis
Article Snippet: .. For detection of CXCL9 and CXCL10, longitudinal sections were fixed with 4% paraformaldehyde for 20 min, treated with 1% Triton X-100 in PBS at room temperature, blocked for 30 min, and then stained with rabbit anti-mouse laminin (Cedarlane Laboratories, Ontario, Canada), rat anti-mouse CD138 (BD Bioscience), goat anti-mouse CXCL9 (AF492-NA; R&D Systems), goat anti-mouse CXCL10 (AF-466-NA; R&D Systems), rat anti-mouse glial fibrillary acidic protein (GFAP) (2.2B10; Invitrogen), rabbit anti-mouse ionized calcium binding adaptor molecule-1 (Iba-1) (Wako, Richmond, VA), anti-mouse CD31 (550274; BD Bioscience), or anti-JHMV monoclonal Ab overnight at 4°C. ..

Article Title: A Therapeutic OX40 Agonist Dynamically Alters Dendritic, Endothelial, and T Cell Subsets within the Established Tumor Microenvironment
Article Snippet: .. The following primary antibodies used for staining sections: rat anti-mouse CD31 (BD ences), goat anti-mouse OX40 (Santa Cruz Biotechnolat anti-mouse OX40 (eBioscience), hamster anti-mouse (BD Biosciences), rat anti-mouse VCAM-1 (Santa Cruz hnology), and goat anti-mouse CXCL9 (R&D Systems). llowing secondary antibodies were used: donkey antixa Fluor 488 (Molecular Probes), donkey anti-goat Cy3 on ImmunoResearch), donkey anti-hamster Alexa Flu(Molecular Probes), donkey anti-rat Cy3 (Jackson ImResearch), goat anti-rat Fab1 fragment Cy3 (Jackson noResearch), and goat anti-rat Alexa Fluor 488 (Molecrobes). .. All sections were briefly incubated with 4′,6- ino-2-phenylindole (DAPI; Sigma) and then mounted. s were acquired using an Olympus FluoView 1000 al microscope (Olympus).

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Article Title: Astrocyte-Derived CXCL10 Drives Accumulation of Antibody-Secreting Cells in the Central Nervous System during Viral Encephalomyelitis
Article Snippet: .. For detection of CXCL9 and CXCL10, longitudinal sections were fixed with 4% paraformaldehyde for 20 min, treated with 1% Triton X-100 in PBS at room temperature, blocked for 30 min, and then stained with rabbit anti-mouse laminin (Cedarlane Laboratories, Ontario, Canada), rat anti-mouse CD138 (BD Bioscience), goat anti-mouse CXCL9 (AF492-NA; R&D Systems), goat anti-mouse CXCL10 (AF-466-NA; R&D Systems), rat anti-mouse glial fibrillary acidic protein (GFAP) (2.2B10; Invitrogen), rabbit anti-mouse ionized calcium binding adaptor molecule-1 (Iba-1) (Wako, Richmond, VA), anti-mouse CD31 (550274; BD Bioscience), or anti-JHMV monoclonal Ab overnight at 4°C. ..

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Measurement of CTL activity and IFN-γ release in mice treated with IL13-PE and IL-13Rα2 DNA. Splenocytes restimulated with mitomycin C-treated 4T1 (A) or MCA304 (B) tumor cells for 1 wk in culture medium containing IL-2 (20 IU/ml) were used as effector cells. 4T1 or MCA304 target cells were labeled with [51Cr] for 2 h, washed thrice, and then plated into 96-well plates with effector cells. Specific lysis was calculated, as described in Materials and Methods, after 4 h of culture. Culture supernatants of splenocytes restimulated with mitomycin C-treated 4T1 (C) or MCA304 (D) tumor cells for 48 h were assessed by ELISA for murine IFN-γ production. D5 melanoma and CT-26 were used as negative control. Spleens from five mice were harvested. Data presented are representative of two independent experiments with similar results. Bars, SD. Statistical analysis was performed using oneway ANOVA. The difference between DNA vaccine and combination therapy group in IFN-γ ELISA assay in the 4T1 tumor model was statistically significant at p < 0.001 (C). Similarly, the difference between either DNA vaccine alone or IL13-PE alone and combination therapy was statistically significant at p < 0.001 in the MCA304 tumor model (D).

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: A Novel Combination Immunotherapy for Cancer by IL-13R?2-Targeted DNA Vaccine and Immunotoxin in Murine Tumor Models

doi: 10.4049/jimmunol.1102095

Figure Lengend Snippet: Measurement of CTL activity and IFN-γ release in mice treated with IL13-PE and IL-13Rα2 DNA. Splenocytes restimulated with mitomycin C-treated 4T1 (A) or MCA304 (B) tumor cells for 1 wk in culture medium containing IL-2 (20 IU/ml) were used as effector cells. 4T1 or MCA304 target cells were labeled with [51Cr] for 2 h, washed thrice, and then plated into 96-well plates with effector cells. Specific lysis was calculated, as described in Materials and Methods, after 4 h of culture. Culture supernatants of splenocytes restimulated with mitomycin C-treated 4T1 (C) or MCA304 (D) tumor cells for 48 h were assessed by ELISA for murine IFN-γ production. D5 melanoma and CT-26 were used as negative control. Spleens from five mice were harvested. Data presented are representative of two independent experiments with similar results. Bars, SD. Statistical analysis was performed using oneway ANOVA. The difference between DNA vaccine and combination therapy group in IFN-γ ELISA assay in the 4T1 tumor model was statistically significant at p < 0.001 (C). Similarly, the difference between either DNA vaccine alone or IL13-PE alone and combination therapy was statistically significant at p < 0.001 in the MCA304 tumor model (D).

Article Snippet: Slides were incubated with rat anti-mouse CD4 Ab (1 µg/ml; MCA1767; Serotec, Oxford, U.K.); rat anti-mouse CD8 Ab (1 µg/ml; MCA1108G; Serotec); goat anti-mouse monokine induced by IFN-γ (MIG/CXCL9) (1 µg/ml; R&D Systems) Ab; rabbit anti-mouse IFN-γ–inducible protein-10 (IP-10/CXCL10) (1 µg/ ml; PeproTech, Rocky Hill, NJ) Ab; rat anti-CXCR3, CD11b, and Gr-1 Ab (5 µg/ml; eBioscience); mouse anti–arginase-1 Ab (5 µg/ml; BD Bioscience); rabbit anti–NO synthase-2 Ab (5 µg/ml; Santa Cruz Biotechnology); or isotype control for 18 h at 4°C.

Techniques: Activity Assay, Labeling, Lysis, Enzyme-linked Immunosorbent Assay, Negative Control

Detection of CD4+ and CD8+ T cells and chemokines in regressing tumors of treated mice. The 4T1 tumor samples in mice receiving PBS, IL13-PE alone, IL-13Rα2 DNA alone, and the combination therapy of IL13-PE and IL-13Rα2 DNA were collected on day 33 from the experiment shown in Fig. 1B. A, The immunofluorescence microscopic analyses of tumors from three mice were done using Abs specific for CD4, CD8, CXCL9, CXCL10 (IP-10), and CXCR3. The representative images of a tumor from each group are shown. Scale bars, 50 µm. Original magnification ×400. B, The number of CD4+ (upper panel) or CD8+ (lower panel) cells (per ×400 field of view) was counted in each group. A total of six fields was counted for each area. C–E, Role of host-immune cells in combination therapy-induced 4T1 and MCA304 tumor growth inhibition. CD4+ and/or CD8+ T cells or NK cells were depleted in the mice receiving combination therapy with IL13-PE and IL-13Rα2 DNA in 4T1 (C) and MCA304 (D) tumor models. For CD4+ and CD8+ depletion, mice were injected i.p. with 0.25 mg of anti-CD4 Ab (GK1.5) and/or 0.2 mg of anti-CD8 Ab (2.43) on days −2, −1, (Figure legend continues) 5, 11, and 17 relative to the tumor implantation. NK cells were depleted with rabbit anti–asialo-GM1 Ab (50 µg/injection) on the same days as CD4+, CD8+ T cell depletion (E). RAG-2 knockout or wild-type C57BL/6 mice bearing MCA304 tumor received combination therapy. Each group contained five or six mice.

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: A Novel Combination Immunotherapy for Cancer by IL-13R?2-Targeted DNA Vaccine and Immunotoxin in Murine Tumor Models

doi: 10.4049/jimmunol.1102095

Figure Lengend Snippet: Detection of CD4+ and CD8+ T cells and chemokines in regressing tumors of treated mice. The 4T1 tumor samples in mice receiving PBS, IL13-PE alone, IL-13Rα2 DNA alone, and the combination therapy of IL13-PE and IL-13Rα2 DNA were collected on day 33 from the experiment shown in Fig. 1B. A, The immunofluorescence microscopic analyses of tumors from three mice were done using Abs specific for CD4, CD8, CXCL9, CXCL10 (IP-10), and CXCR3. The representative images of a tumor from each group are shown. Scale bars, 50 µm. Original magnification ×400. B, The number of CD4+ (upper panel) or CD8+ (lower panel) cells (per ×400 field of view) was counted in each group. A total of six fields was counted for each area. C–E, Role of host-immune cells in combination therapy-induced 4T1 and MCA304 tumor growth inhibition. CD4+ and/or CD8+ T cells or NK cells were depleted in the mice receiving combination therapy with IL13-PE and IL-13Rα2 DNA in 4T1 (C) and MCA304 (D) tumor models. For CD4+ and CD8+ depletion, mice were injected i.p. with 0.25 mg of anti-CD4 Ab (GK1.5) and/or 0.2 mg of anti-CD8 Ab (2.43) on days −2, −1, (Figure legend continues) 5, 11, and 17 relative to the tumor implantation. NK cells were depleted with rabbit anti–asialo-GM1 Ab (50 µg/injection) on the same days as CD4+, CD8+ T cell depletion (E). RAG-2 knockout or wild-type C57BL/6 mice bearing MCA304 tumor received combination therapy. Each group contained five or six mice.

Techniques: Immunofluorescence, Inhibition, Injection, Tumor Implantation, Knock-Out

Figure 4. MM growth and post-transplantation therapy strongly increase the expression of inﬂammatory chemokines and IFN-g in the BM. (A) mRNA levels of the inﬂammatory chemokines CXCL9, CXCL10, CXCL11, and CXCL16 and the homeostatic chemokine CXCL12 in the BM (femurs and tibias) of the experimental groups. (B) Chemokine mRNA levels in ex vivo MM cells (n ¼ 2) sorted from the BM of BMT MM mice. (C) mRNA expression levels of CXCL9 and CXCL16 protein in the experimental groups. (D) mRNA expression levels of proinﬂammatory cytokine IFN-g in the experimental groups. mRNA levels were determined by qPCR; protein levels, by ELISA. Data are the combined results of at least 3 analyses, with 5-10 mice analyzed per group. P values <.05 are shown below each panel.

Journal: Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

Article Title: Homing characteristics of donor T cells after experimental allogeneic bone marrow transplantation and posttransplantation therapy for multiple myeloma.

doi: 10.1016/j.bbmt.2012.12.014

Figure Lengend Snippet: Figure 4. MM growth and post-transplantation therapy strongly increase the expression of inﬂammatory chemokines and IFN-g in the BM. (A) mRNA levels of the inﬂammatory chemokines CXCL9, CXCL10, CXCL11, and CXCL16 and the homeostatic chemokine CXCL12 in the BM (femurs and tibias) of the experimental groups. (B) Chemokine mRNA levels in ex vivo MM cells (n ¼ 2) sorted from the BM of BMT MM mice. (C) mRNA expression levels of CXCL9 and CXCL16 protein in the experimental groups. (D) mRNA expression levels of proinﬂammatory cytokine IFN-g in the experimental groups. mRNA levels were determined by qPCR; protein levels, by ELISA. Data are the combined results of at least 3 analyses, with 5-10 mice analyzed per group. P values <.05 are shown below each panel.

Article Snippet: In addition, we used mouse anti-heparan sulfate (10E4) [12]; mouse anti-VSV (Sigma-Aldrich, St Louis, MO); goat anti-glypican-1 (Santa Cruz Biotechnology, Santa Cruz, CA); biotinylated goat anti-mouse CXCL9 and CXCL10 (both R&D Systems); FITC-conjugated mouse anti-H-2Db and hamster antiCD11c; Alexa Fluor 488-conjugated goat anti-mouse IgG (Life Technologies), Alexa Fluor 488-conjugated goat anti-mouse IgM (Life Technologies); Alexa Fluor 647-conjugated hamster anti-CD11c (AbD Serotec, Kidlington, UK); PE-conjugated hamster anti-CD80; and control (MPB49) and antichondroitin sulfate single chains (IO3H10) [13].

Techniques: Transplantation Assay, Expressing, Ex Vivo, Enzyme-linked Immunosorbent Assay

Figure 5. IFN-g and TNF-a induce the expression of inﬂammatory chemokines by BMECs. mRNA levels of the chemokines CXCL9, CXCL10, CXCL11, CXCL12, and CXCL16 in BMEC STR-12 were determined by qPCR. BMECs were cultured in the presence of the indicated concentrations of IFN-g, TNF-a, or IFN-g plus 10 ng/mL TNF-a for 2 days. Data are mean SD of duplicates. Results are representative of 2 experiments. AU, arbitrary units.

Journal: Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

Article Title: Homing characteristics of donor T cells after experimental allogeneic bone marrow transplantation and posttransplantation therapy for multiple myeloma.

doi: 10.1016/j.bbmt.2012.12.014

Figure Lengend Snippet: Figure 5. IFN-g and TNF-a induce the expression of inﬂammatory chemokines by BMECs. mRNA levels of the chemokines CXCL9, CXCL10, CXCL11, CXCL12, and CXCL16 in BMEC STR-12 were determined by qPCR. BMECs were cultured in the presence of the indicated concentrations of IFN-g, TNF-a, or IFN-g plus 10 ng/mL TNF-a for 2 days. Data are mean SD of duplicates. Results are representative of 2 experiments. AU, arbitrary units.

Techniques: Expressing, Cell Culture

Figure 6. BMECs present inﬂammatory chemokines on multiple HSPGs. (A) BMECs show high expression of heparan sulfate on staining with anti-heparan sulfate (bold line) versus isotype control (stippled line). (B) RT-PCR with a panel of HSPG-speciﬁc primers shows expression of 8 of 11 HSPGs by BMECs. (C) BMEC surface expression of syndecans-1, syndecans-4, and glypicans-1 (bold lines) versus isotype controls (stippled lines), as determined by ﬂow cytometry. (D) BMECs were loaded with CXCL9 or CXCL10, washed, and analyzed by ﬂow cytometry for the presence of the chemokines. (E) Expression of heparan sulfate (HS) and chondroitin sulfate (CS) with or without enzymatic treatment of BMECs (left). BMEC-bound CXCL9 and CXCL10 are released on the cleavage of heparan sulfate by heparinases, but not after removal of chondroitin sulfate (right). Relative expression is in delta mean ﬂuorescence intensity (MFI) means MFI of the speciﬁc marker minus isotype control. One representative experiment out of 3 experiments is shown.

Journal: Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

Article Title: Homing characteristics of donor T cells after experimental allogeneic bone marrow transplantation and posttransplantation therapy for multiple myeloma.

doi: 10.1016/j.bbmt.2012.12.014

Figure Lengend Snippet: Figure 6. BMECs present inﬂammatory chemokines on multiple HSPGs. (A) BMECs show high expression of heparan sulfate on staining with anti-heparan sulfate (bold line) versus isotype control (stippled line). (B) RT-PCR with a panel of HSPG-speciﬁc primers shows expression of 8 of 11 HSPGs by BMECs. (C) BMEC surface expression of syndecans-1, syndecans-4, and glypicans-1 (bold lines) versus isotype controls (stippled lines), as determined by ﬂow cytometry. (D) BMECs were loaded with CXCL9 or CXCL10, washed, and analyzed by ﬂow cytometry for the presence of the chemokines. (E) Expression of heparan sulfate (HS) and chondroitin sulfate (CS) with or without enzymatic treatment of BMECs (left). BMEC-bound CXCL9 and CXCL10 are released on the cleavage of heparan sulfate by heparinases, but not after removal of chondroitin sulfate (right). Relative expression is in delta mean ﬂuorescence intensity (MFI) means MFI of the speciﬁc marker minus isotype control. One representative experiment out of 3 experiments is shown.

Techniques: Expressing, Staining, Control, Reverse Transcription Polymerase Chain Reaction, Cytometry, Marker

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