1
Egins with dengue infection of dendritic cells that, in turn, promiscuously activates T cells. T cells during a dengue infection have prolific and cross reactive effector functions in addition to producing copious amounts of cytokines that feature prominently in cases of DHF/DSS. A second component in immune enhancement is Antibody Dependant Enhancement (ADE). Heterologus non-neutralizing antibodi
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Ells can increase viral RNA production by over 100-fold making dendritic cells potent components in dengue pathogenesis[20]. Infected dendritic cells also contribute to vascular leak through the production of matrix metalloproteinases (MMPs). MMP-2, MMP-13, and MMP-9 were all dramatically increased in immature dendritic cells infected with DENV2. As a result cell-cell adhesion in cells co-cultured
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Izes DHF/DSS are regulated by Complement proteins and associated anaphylatoxins. These three systems both interact and reinforce each other to create a potentially life threatening situation during a Dengue infection.Antibodies Antibody Dependent Enhancement (ADE) has been proposed to be a mechanism by which the immune system may enhance viral pathogenesis[7]. When monkeys were passively immunized
1
The antibodies are involved in release of complement and anaphylatoxins which can cause or exacerbate DHF/DSS. These systems are inextricable and strongly associated with dengue pathogenesis.Dengue Background and SignificanceThe Dengue Virus is a member of the family Flaviviridae along with other noted viruses Yellow Fever, West Nile, and Japanese Encephalitis. Dengue is a positive stranded RNA ar
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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
1
Egins with dengue infection of dendritic cells that, in turn, promiscuously activates T cells. T cells during a dengue infection have prolific and cross reactive effector functions in addition to producing copious amounts of cytokines that feature prominently in cases of DHF/DSS. A second component in immune enhancement is Antibody Dependant Enhancement (ADE). Heterologus non-neutralizing antibodi
1
Izes DHF/DSS are regulated by Complement proteins and associated anaphylatoxins. These three systems both interact and reinforce each other to create a potentially life threatening situation during a Dengue infection.Antibodies Antibody Dependent Enhancement (ADE) has been proposed to be a mechanism by which the immune system may enhance viral pathogenesis[7]. When monkeys were passively immunized
1
Cytosis and the immune enhancement are reduced with abrogated cell signaling. The disparity is not yet understood. It does suggest that viral entry and immune enhancement can be mediated by more than a single mechanism. In a different study, three cell types have been used to demonstrate enhancement[16]. U9357 cells which express both FcRIIA and FcRI have similar antibody-dependent enhancement cap

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