1
Anti-NS1 antibodies stimulating the release of IL-6, IL-8, and MCP-1 in an NFB-dependent manner. Correlated with antibody binding is the upregulation of ICAM1. ICAM1 upregulation can facilitate the adherence of PBMCs to the endothelium. Both NFB inhibitors and soluble NS1 to block the antiNS1 antibodies can able to block cytokine release in vitro[46]. Using ELISA flow cytometry, it can be shown th
1
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
1
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
1
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
1
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
1
Ivation is greatly enhanced. When they added purified NS1 protein to normal or convalescent sera they found synonymous results with NS1 activating complement and complement activation being synergized by anti-dengue antibodies. While NS1 could clearly activate complement in the fluid phase it was unable activate complement when stably expressed on the surface of cells. However, when patient sample
1
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
1
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

Social Bookmarking Sites
What is Kliqqi?

Kliqqi is an open source content management system that lets you easily create your own user-powered website.

Latest Comments