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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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D increases permeability of small blood vessels and smooth muscle contraction. In macrophages, eosinophiles, and neutrophils anaphylatoxins can induce oxidative burst, basophiles, and mast cells release histamine, and C3a can enhance the effect of other proinflammatory cytokines such as TNF, IL-6, and SDF-1. While the mechanism for the many reactions precipitated by complement anaphylatoxins has n
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Ls. Activation of effector T-cells and secretion of cytokines define a key development in course of disease associated with dengue virus infection. Four patient studies done in Vietnam[28], India[29], Cuba[30], and Brazil[31] all showed increases in INF, TNF, IL-10, IL-1, IL-6, IL-8, and MCP1 amongst a variety of other cytokines. In vitro studies, IFN, IL-6, TNF, and RANTES upregulation also have
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Om neutrophils, eosinophiles, and basophiles. C3a and C5a act on specific receptors to produce local inflammatory responses and when secreted in concentrations high enough to invoke a general systemic response, they cause circulatory collapse similar to an IgE mediated allergic response. ATs modulate the secretion of IL-6, and TNF from B cells and serve as potent chemoattractants[52]. C5a also wor
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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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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