A5023533946- Dermatology and Skin Diseases
- Allergic Rhinitis and Sensitization
- Urticaria and Related Conditions
- Asthma and respiratory diseases
- Autoimmune Bullous Skin Diseases
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Contact Dermatitis and Allergies
- Psoriasis: Treatment and Pathogenesis
- Immune Cell Function and Interaction
- Cutaneous lymphoproliferative disorders research
- Food Allergy and Anaphylaxis Research
- Cancer and Skin Lesions
- Mast cells and histamine
- Drug-Induced Adverse Reactions
- Nail Diseases and Treatments
- Skin and Cellular Biology Research
- Eosinophilic Disorders and Syndromes
- IL-33, ST2, and ILC Pathways
- Immune Response and Inflammation
- Dermatological and Skeletal Disorders
- Hedgehog Signaling Pathway Studies
- Nonmelanoma Skin Cancer Studies
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Vascular Tumors and Angiosarcomas
Singapore Immunology Network
2016-2025
Agency for Science, Technology and Research
2016-2025
Kyoto University
2016-2025
A*STAR Graduate Academy
2024
Japanese Urological Association
2024
Sungkyunkwan University
2020-2023
National Skin Centre
2019-2023
Institute of Medical Biology
2015-2022
Kyoto University Hospital
2015-2022
Weatherford College
2020
Tissue macrophages have a split personality Resident tissue (RTMs) reside in various tissue-specific niches during development. They evince microenvironment-directed phenotypes that support host defense and homeostasis. Chakarov et al. used single-cell RNA sequencing fate-mapping of murine lung RTMs to interrogate RTM-subset heterogeneity, interrelationships, ontogeny (see the Perspective by Mildner Yona). In addition alveolar macrophages, they identified two different interstitial...
Allergic asthma is caused by the aberrant expansion in lung of T helper cells that produce type 2 (T H 2) cytokines and characterized infiltration eosinophils bronchial hyperreactivity. This disease often triggered mast activated immunoglobulin E (IgE)–mediated allergic challenge. Activated release various chemical mediators, including prostaglandin D (PGD ), whose role has now been investigated generation mice deficient PGD receptor (DP). Sensitization aerosol challenge homozygous mutant...
Abstract BACKGROUND: Melanoma tends to be refractory various immunotherapies because of tumor‐induced immunosuppression. To investigate the mechanism underlining immunosuppression melanoma patients, authors focused on programmed cell death‐1 (PD‐1)/PD‐1 ligand 1 (PD‐L1) interaction between tumor cells and T cells. METHODS: specimens were collected from 59 primary tumors, 16 lymph nodes, 4 lesions in‐transit metastasis. Specimens stained with anti‐PD‐L1 monoclonal antibodies digitalized jpg...
Interleukin-31 may play a role in the pathobiologic mechanism of atopic dermatitis and pruritus. We wanted to assess efficacy safety nemolizumab (CIM331), humanized antibody against interleukin-31 receptor A, treatment dermatitis.In this phase 2, randomized, double-blind, placebo-controlled, 12-week trial, we assigned adults with moderate-to-severe that was inadequately controlled by topical treatments receive subcutaneous (at dose 0.1 mg, 0.5 or 2.0 mg per kilogram body weight) placebo...
We used mice deficient in each of the eight types and subtypes prostanoid receptors examined roles prostanoids dextran sodium sulfate–induced (DSS-induced) colitis. Among receptor–deficient mice, only EP4-deficient not either DP, EP1, EP2, EP3, FP, IP, or TP developed severe colitis with 3% DSS treatment, which induced marginal wild-type mice. This phenotype was mimicked by administration an EP4-selective antagonist (AE3-208). The EP4 deficiency impaired mucosal barrier function epithelial...
We used mice deficient in each of the eight types and subtypes prostanoid receptors examined roles prostanoids dextran sodium sulfate–induced (DSS-induced) colitis. Among receptor–deficient mice, only EP4-deficient not either DP, EP1, EP2, EP3, FP, IP, or TP developed severe colitis with 3% DSS treatment, which induced marginal wild-type mice. This phenotype was mimicked by administration an EP4-selective antagonist (AE3-208). The EP4 deficiency impaired mucosal barrier function epithelial...
Background Baricitinib, an oral selective Janus kinase 1 and 2 inhibitor, effectively reduced atopic dermatitis (AD) severity in a phase II study with concomitant topical corticosteroids. Objectives To evaluate the efficacy safety of baricitinib patients moderate-to-severe AD who had inadequate response to therapies. Methods In two independent, multicentre, double-blind, III monotherapy trials, BREEZE-AD1 BREEZE-AD2, adults were randomized : once-daily placebo, mg, or 4 mg for 16 weeks....
Tregs play an important role in protecting the skin from autoimmune attack. However, extent of Treg trafficking between and draining lymph nodes (DLNs) is unknown. We set out to investigate this using mice engineered express photoconvertible fluorescence protein Kaede, which changes green red when exposed violet light. By exposing Kaede-transgenic light, we were able label T cells periphery under physiological conditions with Kaede-red demonstrated that both memory phenotype CD4+Foxp3–...
Nemolizumab is a subcutaneously administered humanized monoclonal antibody against interleukin-31 receptor A, which involved in pruritus and inflammation atopic dermatitis. In phase 2 studies, nemolizumab lessened the severity of
Baricitinib, an oral selective Janus kinase 1 and 2 inhibitor, effectively reduced disease severity in moderate to severe atopic dermatitis (AD) phase 3 monotherapy studies.