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N, however, when cells were exposed to heterologus antigens they produced significantly higher amounts of TNF in relation to IFN[41]. During primary infections in mice, dengue specific CD4+ cells were low; however, in all four viral serotypes of a secondary infection there is a marked increase CD4+ response. Not only did CD4+ cells increase IFN production, but they increased CD8+ effector cell act
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Ic cells have been shown to attenuate the immune response and promote tolerance in a way analogous to Tregulatory cells. DCs can also activate B-cells through costimulation of CD40, IL-6, and IL-12. The crux of DC interaction is in two places: DC maturation and T-cell synapse. Either point represents a potential target for dengue virus immune evasion. Should DCs fail to mature properly, they will
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Ic cells have been shown to attenuate the immune response and promote tolerance in a way analogous to Tregulatory cells. DCs can also activate B-cells through costimulation of CD40, IL-6, and IL-12. The crux of DC interaction is in two places: DC maturation and T-cell synapse. Either point represents a potential target for dengue virus immune evasion. Should DCs fail to mature properly, they will
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Ic cells have been shown to attenuate the immune response and promote tolerance in a way analogous to Tregulatory cells. DCs can also activate B-cells through costimulation of CD40, IL-6, and IL-12. The crux of DC interaction is in two places: DC maturation and T-cell synapse. Either point represents a potential target for dengue virus immune evasion. Should DCs fail to mature properly, they will
1
Ic cells have been shown to attenuate the immune response and promote tolerance in a way analogous to Tregulatory cells. DCs can also activate B-cells through costimulation of CD40, IL-6, and IL-12. The crux of DC interaction is in two places: DC maturation and T-cell synapse. Either point represents a potential target for dengue virus immune evasion. Should DCs fail to mature properly, they will
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Anti-NS1 antibodies stimulating the release of IL-6, IL-8, and MCP-1 in an NFB-dependent manner. Correlated with antibody binding is the upregulation of ICAM1. ICAM1 upregulation can facilitate the adherence of PBMCs to the endothelium. Both NFB inhibitors and soluble NS1 to block the antiNS1 antibodies can able to block cytokine release in vitro[46]. Using ELISA flow cytometry, it can be shown th
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At typically binds to IgG and is composed of an chain for domain recognition, an ITAM (immunoreceptor tyrosine based activation motif), and a chain that is responsible for signal transduction. It is thought that IgM does not play a direct role in ADE and instead contributes to disease pathogenesis through activation of complement receptors[13]. IgM antibody enhancement was abrogated when C3R is
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At typically binds to IgG and is composed of an chain for domain recognition, an ITAM (immunoreceptor tyrosine based activation motif), and a chain that is responsible for signal transduction. It is thought that IgM does not play a direct role in ADE and instead contributes to disease pathogenesis through activation of complement receptors[13]. IgM antibody enhancement was abrogated when C3R is