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Yasuda, Kei

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

Property	Value
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	plasmacytoid dendritic cells

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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

plasmacytoid dendritic cells

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

Item Type	Name
Concept	Dendritic Cells
Academic Article	Efficient uptake and rapid degradation of plasmid DNA by murine dendritic cells via a specific mechanism.
Academic Article	Endosomal translocation of vertebrate DNA activates dendritic cells via TLR9-dependent and -independent pathways.
Academic Article	The uptake and degradation of DNA is impaired in macrophages and dendritic cells from NZB/W F(1) mice.
Academic Article	CpG motif-independent activation of TLR9 upon endosomal translocation of "natural" phosphodiester DNA.
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	DNA-like class R inhibitory oligonucleotides (INH-ODNs) preferentially block autoantigen-induced B-cell and dendritic cell activation in vitro and autoantibody production in lupus-prone MRL-Fas(lpr/lpr) mice in vivo.
Academic Article	Requirement for DNA CpG content in TLR9-dependent dendritic cell activation induced by DNA-containing immune complexes.
Academic Article	Phenotype and function of B cells and dendritic cells from interferon regulatory factor 5-deficient mice with and without a mutation in DOCK2.
Academic Article	Inhibition of IRF4 in dendritic cells by PRR-independent and -dependent signals inhibit Th2 and promote Th17 responses.

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dendritic cells