Fig. 1.
Fig. 1. IFN-γ–mediated increase of transient calcium flux in response to RANTES (ligand to CRs, including CCR1, CCR3, CCR4, and CCR5), MIP-1α (ligand to CRs, including CCR1, CCR4, and CCR5), MIP1-β (a ligand to CCR5), and SDF-1 (a ligand to CXCR4) as assessed in U937 cells. Fluorescence of bound versus unbound intracellular calcium in response to chemokines as depicted was analyzed by flow cytometry14 3 (left panel) and 5 days (right panel) after treatment with IFN-γ, as compared with untreated control cells (representative of 5 independent experiments).

IFN-γ–mediated increase of transient calcium flux in response to RANTES (ligand to CRs, including CCR1, CCR3, CCR4, and CCR5), MIP-1α (ligand to CRs, including CCR1, CCR4, and CCR5), MIP1-β (a ligand to CCR5), and SDF-1 (a ligand to CXCR4) as assessed in U937 cells. Fluorescence of bound versus unbound intracellular calcium in response to chemokines as depicted was analyzed by flow cytometry14 3 (left panel) and 5 days (right panel) after treatment with IFN-γ, as compared with untreated control cells (representative of 5 independent experiments).

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