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Search Results to Kei Yasuda, PhD

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One or more keywords matched the following properties of Yasuda, Kei

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Research Expertise & Professional Interests “To the clinician, systemic lupus erythematosus is important because it is a potentially fatal disease that is easily confused with many other disorders. To the immunologist, lupus is intriguing because all the key components of the immune system are involved in the underlying mechanisms of the disease.”(Anisur Rahman, Ph.D., and David A. Isenberg, M.D. N Engl J Med. 2008 Feb 28;358(9):929-39.). I have studied this devastating but intellectually challenging disease more than 10 years. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of great diversity of autoantibodies against nucleic acids (DNA and RNA) and other autoantigens. The autoantibodies form immune complexes that deposit in various tissues including the kidney, causing inflammation and end-organ damage. Current medications are only partially effective and have severe side effects. My recent interest is neutrophil activation induced by immune complexes. Studies have shown that neutrophils release reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) upon stimulation with RNA-containing immune complexes. My new goal is to investigate whether other immune complexes from SLE patients can activate neutrophils, and what kind of signaling pathways are involved in the activation. I am also interested in the role of interferon regulatory factor-5 (IRF5) in the pathogenesis of SLE. Genetic studies have shown that mutations of IRF5 are associated with the disease severity of SLE. Using IRF5-deficient mice and lupus-prone mice, we have shown that IRF5 is a critical regulatory of SLE. In addition, we have shown that sera from SLE patients are able to activate plasmacytoid dendritic cells (pDC) to induce type I IFN , which is a pathogenic cytokines in SLE. We demonstrated that the type I IFN production from pDC is dependent on toll-like receptor-7 (TLR7) and IRF5. We investigate whether IRF5 is involved in the activation of B cells and T cells.
Self-Described Keywords Toll-like receptor-9
Self-Described Keywords Toll-like receptor-7

One or more keywords matched the following items that are connected to Yasuda, Kei

Item TypeName
Concept Toll-Like Receptors
Concept Toll-Like Receptor 2
Concept Toll-Like Receptor 3
Concept Toll-Like Receptor 4
Concept Toll-Like Receptor 7
Concept Toll-Like Receptor 9
Academic Article Restricted cytokine production from mouse peritoneal macrophages in culture in spite of extensive uptake of plasmid DNA.
Academic Article Macrophage activation by a DNA/cationic liposome complex requires endosomal acidification and TLR9-dependent and -independent pathways.
Academic Article Endosomal translocation of vertebrate DNA activates dendritic cells via TLR9-dependent and -independent pathways.
Academic Article CpG motif-independent activation of TLR9 upon endosomal translocation of "natural" phosphodiester DNA.
Academic Article Role of immunostimulatory DNA and TLR9 in gene therapy.
Academic Article DNA and its cationic lipid complexes induce CpG motif-dependent activation of murine dendritic cells.
Academic Article Murine dendritic cell type I IFN production induced by human IgG-RNA immune complexes is IFN regulatory factor (IRF)5 and IRF7 dependent and is required for IL-6 production.
Academic Article TLR4 ligands induce IFN-alpha production by mouse conventional dendritic cells and human monocytes after IFN-beta priming.
Academic Article Murine B cell response to TLR7 ligands depends on an IFN-beta feedback loop.
Academic Article Requirement for DNA CpG content in TLR9-dependent dendritic cell activation induced by DNA-containing immune complexes.
Academic Article Promotion of Inflammatory Arthritis by Interferon Regulatory Factor 5 in a Mouse Model.
Academic Article TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects.
Academic Article Lupus-Associated Immune Complexes Activate Human Neutrophils in an Fc?RIIA-Dependent but TLR-Independent Response.

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  • Toll like receptors