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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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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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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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Helial cells, smooth muscles cells, and activated T-cells, but, interestingly, not na e T-cells. C5aR also activates a number of downstream signaling pathways including PI3K- (Phosophoinosital -3 Kinase), PLC (Phospholipase C), PLD (Phospholipase D), Raf and WASP (Wiskott-Aldrich syndrome protein). As a key modulator of the immune system, complement derived proteins clearly have the capacity to af
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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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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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