The Therapeutic Vaccine Potential of MIS416 Adjuvant - Linking innate and adaptive immunity through the activation of multiple innate host defenses. - BioPharm International

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The Therapeutic Vaccine Potential of MIS416 Adjuvant
Linking innate and adaptive immunity through the activation of multiple innate host defenses.


BioPharm International Supplements


Activating Host Antiviral Defenses


Figure 4. MIS416 induces pDC IFN-α production. Human pDCs were purified from PBMCs using magnetic bead selection of BDCA-2+ cells to high purity and viability. Sorted pDC were cultured at 2.6 x 105 cells/mL in the presence of assay positive control (TLR9 ligand (CpG A ODN 2216; 1 m) or a dose-response of MIS416 for 24 hours. Supernatants were assayed for IFN-α content using flow cytometry cytokine bead array methodology.
Several innate immune responses are considered to be able to contribute to the control of viral infections. These effector mechanisms are multifaceted and include direct antiviral activities and immunomodulatory effects on infected host immune cells that contribute to the elimination of these cells. Direct antiviral activity may comprise soluble factors, such as CD8 antiviral factor (CAF) and IFN-α, which have the capacity to directly affect viral transcription. Although a wide range of other innate cytokines can mediate biologic functions regulating aspects of antiviral immunity, high levels of IFN-α/β appear to be dominant in the context of viral infections and act to regulate other innate responses. The clinical use of IFN-α in treating a variety of viral disorders such as chronic hepatitis B and C, and a broad range of human cancers, lies in its ability to induce a dominant array of antiviral genes that drive pleiotropic host defense pathways that prevent viral replication. Virionyx's MIS416 has been designed to induce both high levels of IFN-α and other key pro-inflammatory cytokines that are clinically relevant to the induction of broad-spectrum innate antiviral immunity. Plasamocytoid dendritic cells demonstrate potent induction of IFN-α following MIS416 uptake (Figure 4). Preclinical studies demonstrate MIS416 is able to inhibit mortality and ameliorate morbidity in a mouse influenza A model when administered following viral exposure (Figure 5).


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