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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 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    chemokine mixture with cxcl2 - by Bioz Stars, 2026-02
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    1) Product Images from "Single-Cell Analysis Reveals Malignant Cells Reshape the Cellular Landscape and Foster an Immunosuppressive Microenvironment of Extranodal NK/T-Cell Lymphoma."

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

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

    doi: 10.1002/advs.202303913

    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).
    Figure Legend 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).

    Techniques Used: Infection, Transformation Assay, Expressing



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    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).
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    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).
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    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).
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    Image Search Results


    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