The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Hexa-acylation and KDO(2)-glycosylation determine the specific immunostimulatory activity of Neisseria meningitidis lipid A for human monocyte derived dendritic cells.

To better understand immune modulation by endotoxin and facilitate the development of novel vaccine adjuvants, the structural requirements of Neisseria meningitidis lipopoly(oligo)saccharide (LOS) for activation of human monocyte derived dendritic cell (MDDC) was determined. Highly purified LOS from wild type and genetically-defined mutants of N. meningitidis serogroup B were used. Unglycosylated or penta-acylated meningococcal KDO(2)-lipid A failed to induce human MDDC maturation and activation. However, both wild type meningococcal LOS and KDO(2)-lipid A, significantly up-regulated CD80, CD83 and CD86 and released significantly higher amounts of IL-12p70, IL-6, IL-10, TNFalpha, MCP-1, IP-10 and RANTES. Further, DCs stimulated with wild type or KDO(2)-lipid A but not meningococcal lipid A or penta-acylated KDO(2)-lipid A stimulated naïve allogeneic CD4+ T cells to secrete enhanced levels of IFN-gamma, relative to T cells primed with immature DCs. In contrast to Escherichia coli LPS, IL-5 production was enhanced or maintained in CD4+ T-cells stimulated with MDDC exposed to wild-type meningococcal LOS and KDO(2)-lipid A. These data suggest that KDO linked to a fully acylated meningococcal lipid A is required for meningococcal endotoxin's immunostimulatory activity of human MDDC via TLR4/MD-2 and that different endotoxin structures influence Th responses mediated by MDDC.[1]

References

 
WikiGenes - Universities