cxcl2 r d systems 276 gb Search Results


recombinant human cxcl2  (R&D Systems)
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R&D Systems recombinant human cxcl2
Staphopain A inhibits CXCR2-mediated calcium mobilization of neutrophils. Fluo-3-labelled neutrophils were preincubated with buffer or 0.5 μM Staphopain A with or without 1 μM Staphostatin A, for 15 min at 37°C. After washing, cells were stimulated with different concentrations of CXCL1 ( A ), CXCL7 ( B ), CXCL8 ( C ), fMLF ( D ), C5a ( E ) or a fixed concentration (3 × 10 −9 M) of <t>CXCL2,</t> CXCL3, CXCL5 and CXCL6 ( F ). To determine the IC 50 (50% of inhibition), Fluo-3-labelled neutrophils were preincubated with different concentrations of Staphopain A for 15 min at 37°C and subsequently stimulated with 3 × 10 −9 M CXCL1 ( G ) or 1 × 10 −8 M CXCL7 ( H ). The IC 50 for CXCL1 and CXCL7 was calculated with the formulas y =−4 E +10 −7 x +4.1314 and y =−3 E +10 −7 x +4.0248, respectively. All figures represent the mean±s.e. of three separate experiments using different donors. The relative calcium mobilization was calculated by dividing the fluorescence after stimulation by the baseline fluorescence. * P <0.05 versus buffer; ** P <0.01 for Staphopain A versus buffer (two-tailed Student's t -test).
Recombinant Human Cxcl2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cxcl2+r+d+systems+276+gb/Recombinant+Human+CXCL2%2FGRO+beta+Protein/pmc03433787-192-10-19
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recombinant human cxcl2 - by Bioz Stars, 2026-10
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chemokine mixture with cxcl2  (R&D Systems)
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R&D Systems chemokine mixture with cxcl2
Figure 7. Schematic diagrams of cross-talks among malignant NK cells and immune cells in the TME of NKTCL. EBV-infected malignant NK cells and immune cells together participate in the development of NKTCL. 1) Upon EBV infection, LMP1 may contribute to the malignant transformation of NK cells (Figure 2H). 2) Malignant NK cells and TAMs secret a variety of chemokines (including CCL2, CCL3, CCL4, CCL5, etc.) and thereby recruit multiple types of immune cells from peripheral blood through corresponding chemotactic interactions (Figure 3A). 3) Soluble DPP4 secreted by malignant NK cells can truncate and rapidly degrade <t>CXCL2,</t> CXCL9, and CXCL10 in NKTCL TME, whereby hampering the recruitment of CXCR2+CXCR3+ immune cells (Figure 3B–H). 4) Malignant NK cells (especially LMP1+ ones) expressing CD86 and PD-L1 can negatively regulate the immune response of tumor-infiltrating T cells including exhausted and regulatory T cells (CD8+ TEX, CD4+ TEX, and Treg; Figures 4A–C and 5A–D). 5) TAMs not only secrete immunosuppressive IL10 and angiogenic VEGFA, but also interact with tumor-infiltrating T cells through suppressive interactions of CD86-CTLA4 and PDL1-PD1 (Figures 4B and 5A).
Chemokine Mixture With Cxcl2, supplied by R&D Systems, 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/product/cxcl2+r+d+systems+276+gb/Recombinant+Human+CXCL2%2FGRO+beta+Protein/pm37949673-401-49-53
Average 92 stars, based on 1 article reviews
chemokine mixture with cxcl2 - by Bioz Stars, 2026-10
92/100 stars
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Staphopain A inhibits CXCR2-mediated calcium mobilization of neutrophils. Fluo-3-labelled neutrophils were preincubated with buffer or 0.5 μM Staphopain A with or without 1 μM Staphostatin A, for 15 min at 37°C. After washing, cells were stimulated with different concentrations of CXCL1 ( A ), CXCL7 ( B ), CXCL8 ( C ), fMLF ( D ), C5a ( E ) or a fixed concentration (3 × 10 −9 M) of CXCL2, CXCL3, CXCL5 and CXCL6 ( F ). To determine the IC 50 (50% of inhibition), Fluo-3-labelled neutrophils were preincubated with different concentrations of Staphopain A for 15 min at 37°C and subsequently stimulated with 3 × 10 −9 M CXCL1 ( G ) or 1 × 10 −8 M CXCL7 ( H ). The IC 50 for CXCL1 and CXCL7 was calculated with the formulas y =−4 E +10 −7 x +4.1314 and y =−3 E +10 −7 x +4.0248, respectively. All figures represent the mean±s.e. of three separate experiments using different donors. The relative calcium mobilization was calculated by dividing the fluorescence after stimulation by the baseline fluorescence. * P <0.05 versus buffer; ** P <0.01 for Staphopain A versus buffer (two-tailed Student's t -test).

Journal: The EMBO Journal

Article Title: Staphylococcus aureus Staphopain A inhibits CXCR2-dependent neutrophil activation and chemotaxis

doi: 10.1038/emboj.2012.212

Figure Lengend Snippet: Staphopain A inhibits CXCR2-mediated calcium mobilization of neutrophils. Fluo-3-labelled neutrophils were preincubated with buffer or 0.5 μM Staphopain A with or without 1 μM Staphostatin A, for 15 min at 37°C. After washing, cells were stimulated with different concentrations of CXCL1 ( A ), CXCL7 ( B ), CXCL8 ( C ), fMLF ( D ), C5a ( E ) or a fixed concentration (3 × 10 −9 M) of CXCL2, CXCL3, CXCL5 and CXCL6 ( F ). To determine the IC 50 (50% of inhibition), Fluo-3-labelled neutrophils were preincubated with different concentrations of Staphopain A for 15 min at 37°C and subsequently stimulated with 3 × 10 −9 M CXCL1 ( G ) or 1 × 10 −8 M CXCL7 ( H ). The IC 50 for CXCL1 and CXCL7 was calculated with the formulas y =−4 E +10 −7 x +4.1314 and y =−3 E +10 −7 x +4.0248, respectively. All figures represent the mean±s.e. of three separate experiments using different donors. The relative calcium mobilization was calculated by dividing the fluorescence after stimulation by the baseline fluorescence. * P <0.05 versus buffer; ** P <0.01 for Staphopain A versus buffer (two-tailed Student's t -test).

Article Snippet: Recombinant mouse KC and human CXCL8 were purchased from Tebu-Bio, recombinant human CXCL2, CXCL3, CXCL5, CXCL6 and CXCL7 from R&D systems. fMLF and recombinant C5a were obtained from Sigma-Aldrich.

Techniques: Concentration Assay, Inhibition, Fluorescence, Two Tailed Test

Figure 7. Schematic diagrams of cross-talks among malignant NK cells and immune cells in the TME of NKTCL. EBV-infected malignant NK cells and immune cells together participate in the development of NKTCL. 1) Upon EBV infection, LMP1 may contribute to the malignant transformation of NK cells (Figure 2H). 2) Malignant NK cells and TAMs secret a variety of chemokines (including CCL2, CCL3, CCL4, CCL5, etc.) and thereby recruit multiple types of immune cells from peripheral blood through corresponding chemotactic interactions (Figure 3A). 3) Soluble DPP4 secreted by malignant NK cells can truncate and rapidly degrade CXCL2, CXCL9, and CXCL10 in NKTCL TME, whereby hampering the recruitment of CXCR2+CXCR3+ immune cells (Figure 3B–H). 4) Malignant NK cells (especially LMP1+ ones) expressing CD86 and PD-L1 can negatively regulate the immune response of tumor-infiltrating T cells including exhausted and regulatory T cells (CD8+ TEX, CD4+ TEX, and Treg; Figures 4A–C and 5A–D). 5) TAMs not only secrete immunosuppressive IL10 and angiogenic VEGFA, but also interact with tumor-infiltrating T cells through suppressive interactions of CD86-CTLA4 and PDL1-PD1 (Figures 4B and 5A).

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Single-Cell Analysis Reveals Malignant Cells Reshape the Cellular Landscape and Foster an Immunosuppressive Microenvironment of Extranodal NK/T-Cell Lymphoma.

doi: 10.1002/advs.202303913

Figure Lengend Snippet: Figure 7. Schematic diagrams of cross-talks among malignant NK cells and immune cells in the TME of NKTCL. EBV-infected malignant NK cells and immune cells together participate in the development of NKTCL. 1) Upon EBV infection, LMP1 may contribute to the malignant transformation of NK cells (Figure 2H). 2) Malignant NK cells and TAMs secret a variety of chemokines (including CCL2, CCL3, CCL4, CCL5, etc.) and thereby recruit multiple types of immune cells from peripheral blood through corresponding chemotactic interactions (Figure 3A). 3) Soluble DPP4 secreted by malignant NK cells can truncate and rapidly degrade CXCL2, CXCL9, and CXCL10 in NKTCL TME, whereby hampering the recruitment of CXCR2+CXCR3+ immune cells (Figure 3B–H). 4) Malignant NK cells (especially LMP1+ ones) expressing CD86 and PD-L1 can negatively regulate the immune response of tumor-infiltrating T cells including exhausted and regulatory T cells (CD8+ TEX, CD4+ TEX, and Treg; Figures 4A–C and 5A–D). 5) TAMs not only secrete immunosuppressive IL10 and angiogenic VEGFA, but also interact with tumor-infiltrating T cells through suppressive interactions of CD86-CTLA4 and PDL1-PD1 (Figures 4B and 5A).

Article Snippet: DPP4 protein (Biolegend; Cat #764102) and the supernatants from NKTCL cells (YT and NK-92) were incubated with DPP4 inhibitor (Linagliptin; Selleck; Cat #S3031) or DMSO (Sigma-Aldrich; Cat #D4540) as control for 1 h, which were then incubated with culture medium without chemokines (PBS) or containing 100 ng mL−1 of chemokine mixture with CXCL2 (R&D Systems, USA; Cat #276-GB-010), CXCL9 (R&D Systems; Cat #392-MG010), and CXCL10 (R&D Systems; Cat #266-IP-010) for a 6-h pretreatment and subsequently added into lower chambers.

Techniques: Infection, Transformation Assay, Expressing