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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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Bited a 325-bp PCR product, whereas SR-AI/II-/- mutant allele showed a 434-bp PCR product. MARCO wild type allele exhibited ca. 500-bp PCR product, and MARCO-/- mutant exhibited ca. 850-bp PCR product. All of the three cell lines are stable and Mycoplasma-free by Mycoplasma PCR ELISA test (Roche, Indianapolis, IN) during culture in the past 24 months.SR-AI/IIM WT ZK1 ZK2 ZK6 MMARCOWT ZK1 ZK2 ZKMAR
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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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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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Mbocytes, and endothelial cells[43]. NS1 is a glycoprotein that is secreted by infected cells, heavily present in patient serum supernatants, lacks a membrane spanning motif, but is not, itself, present in the virus. NS1 is known to be a major immune target and high concentrations of antiNS1 antibodies have been found in severe disease in patient studies[44]. When cells are exposed to NS1 antibodi
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Reactive antibodies activate complement still further. The increase in alternative complement proteins, complement receptors and C protein all facilitate a positive feedback loop that can have dangerous consequences in a dengue infected patient.ConclusionThree immune components interact to produce a confluence of symptoms that define DHF/DSS. Dengue virus initially infects immature dendritic cells
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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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