ArticleScientific reports2017
Disrupting ceramide-CD300f interaction prevents septic peritonitis by stimulating neutrophil recruitment.
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Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
What it found
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Immuno-metabolic dysregulation in type 2 diabetes is associated with altered neutrophil functional plasticity, mitochondrial dysfunction, and compromised responses in sepsis.Journal of translational medicine · 2026Article
- Macrophage TMEM175-Mediated Transcriptional Regulation of Cathepsins Drives Bacterial Killing in Sepsis.Journal of immunology research · 2026Article
- Multi‑omics reveal neutrophil heterogeneity in sepsis (Review).International journal of molecular medicine · 2025Review
- Ceramide signaling in immunity: a molecular perspective.Lipids in health and disease · 2025Review
- Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae.Infection and immunity · 2025Article
- CD300a: An Innate Immune Checkpoint Shaping Tumor Immunity and Therapeutic Opportunity.Cancers · 2025Review
- Intranasal administration of ceramide liposome suppresses allergic rhinitis by targeting CD300f in murine models.Scientific reports · 2024Article
- Functional roles of sphingolipids in immunity and their implication in disease.Experimental & molecular medicine · 2023Review
- Distinct subsets of neutrophils crosstalk with cytokines and metabolites in patients with sepsis.iScience · 2023Article
- CD300b regulates intestinal inflammation and promotes repair in colitis.Frontiers in immunology · 2023Article
- Recent advances in neutrophil chemotaxis abnormalities during sepsis.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2022Review
- Glycolipid Metabolite β-Glucosylceramide Is a Neutrophil Extracellular Trap-Inducing Ligand of Mincle Released during Bacterial Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations.International journal of molecular sciences · 2021Review
- The Expression and Function of CD300 Molecules in the Main Players of Allergic Responses: Mast Cells, Basophils and Eosinophils.International journal of molecular sciences · 2020Review
- Mouse LIMR3/CD300f is a negative regulator of the antimicrobial activity of neutrophils.Scientific reports · 2018Article
- Leukocyte mono-immunoglobulin-like receptor 8 (LMIR8)/CLM-6 is an FcRγ-coupled receptor selectively expressed in mouse tissue plasmacytoid dendritic cells.Scientific reports · 2018Article
- The CD300e molecule in mice is an immune-activating receptor.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 7 institutions in 2 countries.
Kumi IzawaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Akie MaeharaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Masamichi IsobeAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Yuka YasudaAnalytical Science Laboratories, Kao Corporation, Haga, Tochigi, 321-3497, Japan.
Makoto UraiDepartment of Chemotherapy and Mycoses, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8640, Japan.
Yasutaka HoshinoDepartment of Chemotherapy and Mycoses, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8640, Japan.
Keigo UenoDepartment of Chemotherapy and Mycoses, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8640, Japan.
Toshihiro MatsukawaDivision of Cellular Therapy/Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Mariko TakahashiDivision of Cellular Therapy/Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Ayako KaitaniAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Emiko ShibaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Ayako TakamoriAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Shino UchidaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Koichiro UchidaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Keiko MaedaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Nobuhiro NakanoAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Yoshinori YamanishiDivision of Cellular Therapy/Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Toshihiko OkiDivision of Cellular Therapy/Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
David VoehringerDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany.
Axel RoersMedical Faculty "Carl-Gustav Carus", Institute for Immunology, Technische Universität Dresden, Fetscherstraße 74, Dresden, 01307, Germany.
Susumu NakaeLaboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Junko IshikawaAnalytical Science Laboratories, Kao Corporation, Haga, Tochigi, 321-3497, Japan.
Yuki KinjoDepartment of Chemotherapy and Mycoses, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8640, Japan.
Toshiaki ShimizuAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Hideoki OgawaAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Ko OkumuraAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Toshio KitamuraDivision of Cellular Therapy/Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. kitamura@ims.u-tokyo.ac.jp.
Jiro KitauraAtopy Research Center, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. j-kitaura@juntendo.ac.jp.
Juntendo University · JPThe University of Tokyo · JPNational Institute of Infectious Diseases · JPKao Corporation (Japan) · JPCarl Gustav Carus-Institut · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHokkaido University · JP
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a serious clinical problem. Negative regulation of innate immunity is associated with sepsis progression, but the underlying mechanisms remains unclear. Here we show that the receptor CD300f promotes disease progression in sepsis. CD300f
Indexed as
Neutrophil InfiltrationAnimalsAntibodies, MonoclonalBiopsyCeramidesChemotactic FactorsChemotaxis, LeukocyteDisease Models, AnimalImmunoglobulin Fc FragmentsMaleMast CellsMiceMice, KnockoutNeutrophilsPeritonitisReceptors, ImmunologicAntibodies, MonoclonalCeramidesChemotactic FactorsCLM-1 protein, mouseImmunoglobulin Fc FragmentsReceptors, Immunologic
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