Satoshi Uematsu

ORCID: 0000-0002-5347-6737
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Immune Cell Function and Interaction
  • Inflammatory mediators and NSAID effects
  • Immunotherapy and Immune Responses
  • interferon and immune responses
  • NF-κB Signaling Pathways
  • IL-33, ST2, and ILC Pathways
  • Gut microbiota and health
  • Estrogen and related hormone effects
  • Asthma and respiratory diseases
  • T-cell and B-cell Immunology
  • Influenza Virus Research Studies
  • Immune cells in cancer
  • Clostridium difficile and Clostridium perfringens research
  • Eicosanoids and Hypertension Pharmacology
  • Bacteriophages and microbial interactions
  • Viral gastroenteritis research and epidemiology
  • Helicobacter pylori-related gastroenterology studies
  • Antimicrobial Peptides and Activities
  • Eosinophilic Esophagitis
  • Neuropeptides and Animal Physiology
  • Inflammasome and immune disorders
  • Pneumonia and Respiratory Infections
  • Neonatal Respiratory Health Research
  • Pediatric health and respiratory diseases

The University of Tokyo
2016-2025

Osaka Metropolitan University
2022-2025

Genomics (United Kingdom)
2025

Tokyo University of Science
2013-2024

Tokyo Metropolitan University
2022-2024

Osaka City University
2018-2022

Chiba University
2014-2020

University of California, San Diego
2017

Koto Hospital
2017

Osaka University
2006-2015

Raised serum levels of interferon (IFN)-α have been observed in systemic lupus erythematosus (SLE) patients, and these are correlated with both disease activity severity. The origin this IFN-α is still unclear, but increasing evidence suggests the critical involvement activated plasmacytoid predendritic cells (PDCs). In SLE DNA RNA viruses, as well immune complexes (ICs), that consist autoantibodies specific to self-DNA protein particles can stimulate production IFN-α. We developed three...

10.1084/jem.20050914 article EN The Journal of Experimental Medicine 2005-10-17

Malaria parasites within red blood cells digest host hemoglobin into a hydrophobic heme polymer, known as hemozoin (HZ), which is subsequently released the stream and then captured by concentrated in reticulo-endothelial system. Accumulating evidence suggests that HZ immunologically active, but molecular mechanism(s) through modulates innate immune system has not been elucidated. This work demonstrates purified from Plasmodium falciparum novel non-DNA ligand for Toll-like receptor (TLR)9....

10.1084/jem.20041836 article EN The Journal of Experimental Medicine 2005-01-03

One of the factors that contributes to pathogenesis acne is Propionibacterium acnes; yet, molecular mechanism by which P. acnes induces inflammation not known. Recent studies have demonstrated microbial agents trigger cytokine responses via Toll-like receptors (TLRs). We investigated whether TLR2 mediates acnes-induced production in acne. Transfection into a nonresponsive cell line was sufficient for NF-kappa B activation response acnes. In addition, peritoneal macrophages from wild-type,...

10.4049/jimmunol.169.3.1535 article EN The Journal of Immunology 2002-08-01

Fucosylation of intestinal epithelial cells, catalyzed by fucosyltransferase 2 (Fut2), is a major glycosylation mechanism host-microbiota symbiosis. Commensal bacteria induce fucosylation, and fucose used as dietary carbohydrate many these bacteria. However, the molecular cellular mechanisms that regulate induction fucosylation are unknown. Here, we show type 3 innate lymphoid cells (ILC3) induced Fut2 expression in mice. This required cytokines interleukin-22 lymphotoxin commensal...

10.1126/science.1254009 article EN Science 2014-08-22

IFN-β promoter stimulator (IPS)-1 was recently identified as an adapter for retinoic acid–inducible gene I (RIG-I) and melanoma differentiation-associated 5 (Mda5), which recognize distinct RNA viruses. Here we show the critical role of IPS-1 in antiviral responses vivo. IPS-1–deficient mice showed severe defects both RIG-I– Mda5-mediated induction type interferon inflammatory cytokines were susceptible to virus infection. virus–induced regulatory factor-3 nuclear factor κB activation also...

10.1084/jem.20060792 article EN The Journal of Experimental Medicine 2006-06-19

The glycosylphosphatidylinositol (GPI) anchors of Plasmodium falciparum have been proposed to be the major factors that contribute malaria pathogenesis through their ability induce proinflammatory responses. In this study we identified receptors for P. GPI-induced cell signaling leads responses and studied GPI structure-activity relationship. data show is mediated mainly recognition by TLR2 a lesser extent TLR4. activity sn-2-lyso-GPIs comparable with intact GPIs, whereas Man(3)-GPIs about...

10.1074/jbc.m413541200 article EN cc-by Journal of Biological Chemistry 2004-12-29

Toll-like receptors (TLRs) recognize microbial pathogens and trigger innate immune responses. Among TLR family members, TLR7, TLR8, TLR9 induce interferon (IFN)-α in plasmacytoid dendritic cells (pDCs). This induction requires the formation of a complex consisting adaptor MyD88, tumor necrosis factor (TNF) receptor-associated 6 (TRAF6) IFN regulatory (IRF) 7. Here we show an essential role IL-1 kinase (IRAK)-1 TLR7- TLR9-mediated IRF7 signaling pathway. IRAK-1 directly bound phosphorylated...

10.1084/jem.20042372 article EN The Journal of Experimental Medicine 2005-03-14

Activation of TLRs by bacterial products results in rapid activation genes encoding designed to protect the host from perturbing microbes. In intestine, which is colonized a large and diverse population commensal bacteria, TLR signaling may not function simple on/off mode. Here, we show that flagellin receptor TLR5 has an essential nonredundant role protecting gut enteric Mice lacking (TLR5KO mice) developed spontaneous colitis, as assessed well-defined clinical, serologic, histopathologic...

10.1172/jci33084 article EN Journal of Clinical Investigation 2007-11-15
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