Takashi Shichita

ORCID: 0000-0003-1110-1926
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune Response and Inflammation
  • Immune cells in cancer
  • Psoriasis: Treatment and Pathogenesis
  • Immune Cell Function and Interaction
  • S100 Proteins and Annexins
  • T-cell and B-cell Immunology
  • Inflammasome and immune disorders
  • Neurological Disease Mechanisms and Treatments
  • Advanced Glycation End Products research
  • Cardiac Fibrosis and Remodeling
  • IL-33, ST2, and ILC Pathways
  • Cytokine Signaling Pathways and Interactions
  • Acute Ischemic Stroke Management
  • Immunotherapy and Immune Responses
  • Neurogenesis and neuroplasticity mechanisms
  • Cerebrovascular and Carotid Artery Diseases
  • Phagocytosis and Immune Regulation
  • Cardiovascular Health and Disease Prevention
  • Retinal Diseases and Treatments
  • Fatty Acid Research and Health
  • Immunodeficiency and Autoimmune Disorders
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Atherosclerosis and Cardiovascular Diseases
  • NF-κB Signaling Pathways

The University of Tokyo
2023-2024

Tokyo Metropolitan Institute of Medical Science
2017-2024

Tokyo Medical and Dental University
2023-2024

Kyushu University
2005-2024

Japan Agency for Medical Research and Development
2017-2024

Keio University
2009-2017

Japan Science and Technology Agency
2011-2017

National Kyushu Medical Center
2006-2009

Clinical Research Institute
2008

Abstract Inflammasome activation has been implicated in various inflammatory diseases including post-ischaemic inflammation after stroke. Inflammasomes mediate of caspase-1, which subsequently induces secretion pro-inflammatory cytokines such as IL-1β and IL-18, well a form cell death called pyroptosis. In this study, we report that Bruton’s tyrosine kinase (BTK) is an essential component the NLRP3 inflammasome, BTK physically interacts with ASC NLRP3. Inhibition by pharmacological or...

10.1038/ncomms8360 article EN cc-by Nature Communications 2015-06-10

Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. In this review, we focus on post-ischemic triggered by infiltrating immune cells, macrophages, and T lymphocytes. Brain ischemia a sterile organ, but injury-induced mostly dependent Toll-like receptor (TLR) 2 TLR4. Some endogenous TLR ligands, high mobility group box 1 (HMGB1) peroxiredoxin family proteins, particular, are implicated activation inflammatory cytokine expression...

10.3389/fimmu.2012.00132 article EN cc-by Frontiers in Immunology 2012-01-01

Gene therapy may be a promising approach for treatment of brain ischemia, although the efficiency postischemic gene is not established. Our goal in this study was to examine effects transfer interleukin-10 (IL-10), an antiinflammatory cytokine, after induction ischemia.Brain ischemia produced by either photochemical occlusion distal middle cerebral artery focal or bilateral carotid global spontaneously hypertensive rats. Adenoviral vectors encoding human IL-10 (AdIL10) beta-galactosidase...

10.1161/01.cir.0000155622.68580.dc article EN Circulation 2005-02-15

Transplantation of endothelial cells (ECs) is a promising therapeutic approach for ischemic disorders. In addition, the generation ECs has become increasingly important providing vascular plexus to regenerated organs, such as liver. Although many attempts have been made generate from pluripotent stem and nonvascular cells, minimum number transcription factors that specialize in directly inducing remains undefined. Here, by screening 18 are both hematopoietic development, we demonstrate ets...

10.1073/pnas.1413234112 article EN Proceedings of the National Academy of Sciences 2014-12-24

Left ventricular (LV) remodeling leads to chronic heart failure and is a main determinant of morbidity mortality after myocardial infarction (MI). At the present time, therapeutic options prevent LV are limited.We created large MI by permanent ligation coronary artery identified potential link between interleukin (IL)-23/IL-17A axis γδT cells that affects late-stage MI. Despite finsinf infarct size 24 hours surgery was similar in wild-type mice, deficiency IL-23, IL-17A, or improved survival...

10.1161/jaha.112.004408 article EN Journal of the American Heart Association 2012-09-26

Abstract Adoptive T-cell immunotherapy is a promising approach to cancer therapy. Stem cell memory T (T SCM ) cells have been proposed as class of long-lived and highly proliferative cells. CD8 + can be generated in vitro from naive via Wnt signalling; however, methods do not yet exist for inducing activated or Here, we show strategy generating -like (iT cells) CD4 mice humans by coculturing with stromal that express Notch ligand. iT lose PD-1 CTLA-4 expression, produce large number...

10.1038/ncomms15338 article EN cc-by Nature Communications 2017-05-22

Abstract Dendritic cells (DCs) induce immunity and immunological tolerance as APCs. It has been shown that DCs secreting IL-10 IL-10+ Tr1-type regulatory T (Treg) cells, whereas Foxp3-positive Treg are expanded from naive CD4+ by coculturing with mature DCs. However, the mechanism of expansion Foxp3+ not clarified. In this study, we demonstrated suppressors cytokine signaling (SOCS)-3-deficient have a strong potential cell-inducing tolerogenic SOCS3−/− expressed lower levels class II MHC,...

10.4049/jimmunol.179.4.2170 article EN The Journal of Immunology 2007-08-15

Abstract IL-9 is a pleiotropic cytokine that can regulate autoimmune and allergic responses. Th9 cells develop from naive T or Th2 through stimulation by TGF-β in vitro. In this study, we demonstrated Smad2 Smad3 are necessary for production an OVA-induced asthma model using cell–specific Smad2- Smad3-deficient mice. were also redundantly essential signaling to induce histone modifications Il9 transcription. Although Smad2/3 was recruited the promoter stimulation, they not sufficient...

10.4049/jimmunol.1301276 article EN The Journal of Immunology 2013-08-03

Choroidal neovascularization (CNV) is a characteristic of age-related macular degeneration. Genome-wide association studies have provided evidence that the immune system involved in pathogenesis degeneration; however, role inflammatory cytokines CNV has not been established. In this study, we demonstrated IL-17 had strong potential for promoting vascular endothelial growth factor-independent manner laser-induced experimental mice. Infiltrated γδT cells and Thy-1(+) innate lymphoid cells, but...

10.4049/jimmunol.1202495 article EN The Journal of Immunology 2013-01-15

Regulatory T (T reg) cells are central mediators of immune suppression. As such, reg characterized by a distinct pattern gene expression, which includes up-regulation immunosuppressive genes and silencing inflammatory cytokine genes. Although an increasing number transcription factors that regulate have been identified, the mechanisms cell–specific transcriptional program is maintained executed remain largely unknown. The Nr4a family nuclear orphan receptors, we recently identified as...

10.1084/jem.20142088 article EN The Journal of Experimental Medicine 2015-08-24

Abstract Damage-associated molecular patterns (DAMPs) have been implicated in sterile inflammation various tissue injuries. High-mobility group box 1 (HMGB1) is a representative DAMP, and has shown to transmit signals through receptors for advanced glycation end products (RAGEs) TLRs, including TLR2 TLR4. HMGB1 does not, however, bind TLRs with high affinity; therefore, the mechanism of HMGB1-mediated TLR activation remains unclear. In this study, we found that fluorescently labeled was...

10.1093/intimm/dxx010 article EN International Immunology 2017-02-01

Immune responses contribute to tissue injury and repair during after ischemic stroke. However, the spatiotemporal initiating molecular events remain incompletely understood. Here, we show that mice deficient in phosphatidylserine receptor CD300a, which is highly expressed on brain myeloid cells including Ly6Chi monocytes, exhibited ameliorated neurological deficit middle cerebral artery occlusion (MCAO). CD300a inhibited signaling through CD300b-DNAX-activation protein 12 (DAP12) pathway...

10.1126/sciimmunol.abe7915 article EN Science Immunology 2021-10-16
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