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Neutralization. However, in heterotypic dengue virus infections the antibodies are non-neutralizing and lead to enhancement. Two cell lines expressing either FcRIA or FcRIIA have been used to demonstrate that immune complexes can enhance virus infectivity in an FcR mediated fashion. FcRIA is found exclusively on macrophages and dendritic cells and preferentially binds monomeric IgG, while FcRIIA i
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Combine to form a C5 convertase. Runaway complement activation is prevented by binding of Complement Receptor 1 (CR1) and a constitutively active membrane bound Decay Accelerating Factor (DAF, or CD55) which can prevent the complement cascade[51]. In patients with severe dengue, large amounts of C3a have been detected revealing a role for complement in dengue pathogenesis. This finding might be an
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Rough a time consuming and multiphase process that lasts anywhere from 6-24 hours. Adhesion molecules such as ICAM1 and ICAM3 are critical molecules generated by the T-cell during either phase and can bind to the adhesion molecules of DCs particularly DC-SIGN which is a known target of dengue. These molecules are necessary to form a stable synapse between the DC and T-cell[23]. T-cells, in turn, p
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Ts showing FISH EGFR GCN 2.6 (-------) and FISH EGFR GCN
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Fic T-cell response. The mechanism for this is unknown but given the intimacy between DCs and T-cells this represents a potentially productive field of research.The role of T cells in a dengue infectionThere is a clear consensus in the literature about activation of cross-reactive memory T-cells, independent of antibody enhancement, being a pivotal moment in the disease process. As compelling as A
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Are unaffected by the virus. There are yet questions unanswered and the virus continues to spread unabated. However these immune components are several key elements attractive targets for study that hopefully can advance the field of research.12.13. 14. 15. 16.Competing interestsThe author declares that they have no competing interests.Authors' informationsDavid Gentry Nielsen was born 27, Septemb
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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