Showing papers by "Toshiaki Ohteki published in 2013"
TL;DR: The mice lacking CXCL10 or CXCR3 demonstrated improved severity and survival of nonviral and viral ARDS, whereas mice that lack IFNAR1 did not control the severity of ARDS in vivo.
Abstract: Rationale: Patients who developed acute respiratory distress syndrome (ARDS) after infection with severe respiratory viruses (e.g., severe acute respiratory syndrome–coronavirus, H5N1 avian influenza virus), exhibited unusually high levels of CXCL10, which belongs to the non-ELR (glutamic-leucine-arginine) CXC chemokine superfamily. CXCL10 may not be a bystander to the severe virus infection but may directly contribute to the pathogenesis of neutrophil-mediated, excessive pulmonary inflammation.Objectives: We investigated the contribution of CXCL10 and its receptor CXCR3 axis to the pathogenesis of ARDS with nonviral and viral origins.Methods: We induced nonviral ARDS by acid aspiration and viral ARDS by intratracheal influenza virus infection in wild-type mice and mice deficient in CXCL10, CXCR3, IFNAR1 (IFN-α/β receptor 1), or TIR domain-containing adaptor inducing IFN-β (TRIF).Measurements and Main Results: We found that the mice lacking CXCL10 or CXCR3 demonstrated improved severity and survival of no...
243 citations
TL;DR: Collectively, CB promotes IL-10 production by intestinal macrophages in inflamed mucosa, thereby preventing experimental colitis in mice, and the colitis-preventing effect of CB was negated in macrophage-specific IL- 10-deficient mice, suggesting that induction ofIL-10 by intestinal Macrophages is crucial for the probiotic action of CB.
238 citations
TL;DR: These findings provide insight into DC differentiation pathways and may lead to progenitor-based therapeutic applications for infection and autoimmune disease.
179 citations
TL;DR: It is shown that when injected with high Toll-like receptor ligand doses or infected with lymphocytic choriomeningitis virus (LCMV) clone 13, inflammatory monocyte-derived dendritic cells (Mo-DCs) engulfed apoptotic erythroid cells, suggesting that hemophagocytosis moderates immune responses to ensure the host's survival in vivo.
68 citations
TL;DR: It is suggested that CD1c+ mDCs are a major human DC subset that produces RA in response to VD3 in the steady state and may constitute an important immune component for maintaining tissue homeostasis in humans.
Abstract: All-trans-retinoic acid (RA) plays a critical role in maintaining immune homeostasis. Mouse intestinal CD103⁺ dendritic cells (DCs) produce a high level of RA by highly expressing retinal dehydrogenase (RALDH)2, an enzyme that converts retinal to RA, and induce gut-homing T cells. However, it has not been identified which subset of human DCs produce a high level of RA. In this study, we show that CD1c⁺ blood myeloid DCs (mDCs) but not CD141(high) mDCs or plasmacytoid DCs exhibited a high level of RALDH2 mRNA and aldehyde dehydrogenase (ALDH) activity in an RA- and p38-dependent manner when stimulated with 1α,25-dihydroxyvitamin D₃ (VD₃) in the presence of GM-CSF. The ALDH activity was abrogated by TLR ligands or TNF. CD103⁻ rather than CD103⁺ human mesenteric lymph node mDCs gained ALDH activity in response to VD₃. Furthermore, unlike in humans, mouse conventional DCs in the spleen and mesenteric lymph nodes gained ALDH activity in response to GM-CSF alone. RALDH2(high) CD1c⁺ mDCs stimulated naive CD4⁺ T cells to express gut-homing molecules and to produce Th2 cytokines in an RA-dependent manner. This study suggests that CD1c⁺ mDCs are a major human DC subset that produces RA in response to VD₃ in the steady state. The "vitamin D-CD1c⁺mDC-RA" axis may constitute an important immune component for maintaining tissue homeostasis in humans.
29 citations
TL;DR: Type I IFN-based preconditioning, combined with HSC transplantation, is suggested as a novel nongenotoxic treatment of some congenital diseases.
5 citations
01 Jan 2013
01 Jan 2013
TL;DR: This article cites 70 articles, 35 of which you can access for free at: Subscriptions http://jimmunol.org/content/161/11/6030J Immunol€1998; 161:6030-6037.
Abstract: Toshiaki Ohteki and Pamela S. OhashiSanjeev Mariathasan, Martin F. Bachmann, Denis Bouchard,http://www.jimmunol.org/content/161/11/6030J Immunol€1998; 161:6030-6037; ;Referenceshttp://www.jimmunol.org/content/161/11/6030.full#ref-list-1This article cites 70 articles, 35 of which you can access for free at: Subscriptionshttp://jimmunol.org/subscriptionsInformation about subscribing to The Journal of Immunology is online at: Permissionshttp://www.aai.org/ji/copyright.htmlSubmit copyright permission requests at: Email Alertshttp://jimmunol.org/cgi/alerts/etocReceive free email-alerts when new articles cite this article. Sign up at: