5430 research outputs found
Sort by
Production of HIV Gag p24 Monoclonal Antibodies
No full textSlide 4-16: Production of HIV gag p24 monoclonal antibodies to uptake receptors on monocyte-derived dendritic cellshttps://digitalcommons.rockefeller.edu/endocytosis/1014/thumbnail.jp
B16/GalCer Tumor Cells
No full textSlide 5-22: B16/GalCer tumor cells, injected I.V., rapidly mature dendritic cells in an NKT cell-dependent mannerhttps://digitalcommons.rockefeller.edu/nkt-cells/1021/thumbnail.jp
CD1d-EL4/GalCer Injected I.V.
No full textSlide 5-21https://digitalcommons.rockefeller.edu/nkt-cells/1020/thumbnail.jp
A Simple Dose of B16 Melanoma Cells
No full textSlide 5-15: A single dose of B16 melanoma cells, coated with α-Galactosyl ceramide and injected I.V., induces CD8+ T cell immunity to melanoma antigenshttps://digitalcommons.rockefeller.edu/nkt-cells/1014/thumbnail.jp
Dendritic Cells: Targets for Protection and Pathogenesis
No full textSlide 8-2: Dendritic cells: Targets for protection and pathogenesishttps://digitalcommons.rockefeller.edu/sign-family-receptors/1001/thumbnail.jp
Blood-Derived Plasminogen Modulates the Neuroimmune Response in Both Alzheimer\u27s Disease and Systemic Infection Models
Get PDFAlzheimer\u27s disease (AD) is a progressive neurodegenerative disease that affects 44 million people worldwide. To date, there are no effective treatments that prevent progression or death from the disease. It is clear that AD development is multifactorial and can arise from genetic or lifestyle factors and that vascular dysfunction and inflammation play a role in the progression of the disease. Many cardiovascular factors associated with an increase in systemic infection have been linked to a risk of AD development and progression. However, the link between vascular risk factors, systemic inflammation, and the neuroinflammation characteristic of AD are not fully understood. Plasminogen is primarily a blood protein synthesized in the liver, which when cleaved into its active form, plasmin, plays roles in fibrinolysis, wound healing, cell signaling, and inflammatory regulation. Increasing evidence links plasminogen to the regulation of inflammatory responses in many organ systems of the body and implicates plasminogen in the progression of a diverse range of pathologies. I aimed to determine whether plasminogen plays a role in the regulation of neuroinflammation during AD progression. I showed that blood-derived plasmin is a regulator of brain inflammatory activation. Depletion of peripheral plasminogen in an AD mouse model through antisense oligonucleotide (ASO) technology lessened AD pathology and decreased glial cell activation in the brain, whereas an increase in plasmin activity through α2-antiplasmin ASO treatment exacerbated AD mouse pathology. Moreover, blood-derived plasminogen modulated the wild-type mouse brain\u27s neuroinflammatory response to peripheral lipopolysaccharide injection and this was mediated by the p11 receptor, suggesting a more global role for plasminogen in regulating inflammatory communication between the periphery and brain. These studies suggest a crucial role for peripheral plasmin in mediating neuroimmune cell activation and could provide a link to systemic inflammatory risk factors that are known to be associated with the development of AD and other neurological disorders
Innate NKT and MK Cells
No full textSlide 5-4https://digitalcommons.rockefeller.edu/nkt-cells/1003/thumbnail.jp
The Innate and Adaptive Lymphocytes
No full textThe innate and adaptive lymphocytes that recognize distinct targets on or from tumor cellshttps://digitalcommons.rockefeller.edu/nkt-cells/1001/thumbnail.jp
Resistance to B16 Melanoma
No full textSlide 5-14: Resistance to B16 melanoma, following injection of CD1d-B16/GalCer i.v., requires CD4+ and CD8+ cellshttps://digitalcommons.rockefeller.edu/nkt-cells/1013/thumbnail.jp
J558 Plasmacytoma
No full textSlide 5-30https://digitalcommons.rockefeller.edu/nkt-cells/1028/thumbnail.jp