Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: Jan 2, 2026

Murine Model of Epicutaneously-Induced Immunomodulation
09:07

Murine Model of Epicutaneously-Induced Immunomodulation

Published on: June 24, 2025

395

Clec10a regulates mite-induced dermatitis.

Kazumasa Kanemaru1,2, Emiko Noguchi3, Satoko Tahara-Hanaoka1,2,4

  • 1Department of Immunology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.

Science Immunology
|December 8, 2019
PubMed

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Inhibiting glycan degradation prevents HIV-induced inflammaging and cognitive impairment.

Med (New York, N.Y.)·2026
Same author

Correction: Sleep-wake patterns are altered with age, Prdm13 signaling in the DMH and diet restriction in mice.

Life science alliance·2026
Same author

Erratum to "Extracellular polymeric substances in aerobic granular sludge under increasing salinity conditions" [Water Research (2026) 292/125313].

Water research·2026
Same author

TEMIS: A temperature-controlled microwave irradiation system for enhancing extracellular vesicle secretion.

Biochemistry and biophysics reports·2026
Same author

IL-6-driven POU2AF1 and ELL2 are key regulators of multiple myeloma-distinct transcriptional and splicing programs.

Blood advances·2026
Same author

Glycan Markers of Pluripotent Stem Cells.

Advances in experimental medicine and biology·2026
Same journal

Erratum for the Research Article "Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer".

Science immunology·2026
Same journal

Langerhans cell control of early-life dermal lymphatic development shapes adult immunity.

Science immunology·2026
Same journal

T<sub>reg</sub> cells promote immunotherapy-induced immune evasion by restraining CD4 T cell control of MHC-I-deficient metastatic pancreatic cancer.

Science immunology·2026
Same journal

CXCL16-mediated recruitment of γδ T cells to the brain reduces sociability in mice.

Science immunology·2026
Same journal

Bioactive enhanced adjuvant chemokine oligonucleotide nanoparticles (BEACONs) for mucosal vaccination against genital herpes.

Science immunology·2026
Same journal

Bacterial infection reshapes monocyte and macrophage ontogeny at the CNS borders.

Science immunology·2026
See all related articles
Summary
This summary is machine-generated.

A mutation in the Clec10a gene causes hypersensitivity to house dust mites (HDM) and severe dermatitis in mice. Repairing this gene or using its human homolog, Asgr1, can reduce HDM-induced skin inflammation.

Area of Science:

  • Immunology
  • Dermatology
  • Genetics

Background:

  • House dust mite (HDM) allergy is common, causing conditions like atopic dermatitis, but its immune regulation is not fully understood.
  • NC/Nga mice exhibit heightened susceptibility to HDM and develop severe dermatitis, suggesting a genetic basis for their hypersensitivity.

Purpose of the Study:

  • To investigate the genetic mechanisms underlying HDM hypersensitivity in NC/Nga mice.
  • To elucidate the role of C-type lectin receptor Clec10a in regulating immune responses to HDM.
  • To identify human homologs and therapeutic targets for HDM-induced dermatitis.

Main Methods:

  • Whole-exome sequencing to identify mutations in susceptible mouse strains.
  • CRISPR-Cas9 gene editing to repair the identified mutation.

More Related Videos

A Mouse Ear Model for Allergic Contact Dermatitis Evaluation
08:02

A Mouse Ear Model for Allergic Contact Dermatitis Evaluation

Published on: March 24, 2023

4.7K
Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
08:25

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Published on: September 26, 2022

3.4K

Related Experiment Videos

Last Updated: Jan 2, 2026

Murine Model of Epicutaneously-Induced Immunomodulation
09:07

Murine Model of Epicutaneously-Induced Immunomodulation

Published on: June 24, 2025

395
A Mouse Ear Model for Allergic Contact Dermatitis Evaluation
08:02

A Mouse Ear Model for Allergic Contact Dermatitis Evaluation

Published on: March 24, 2023

4.7K
Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
08:25

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Published on: September 26, 2022

3.4K
  • Generation of Clec10a knockout mice (Clec10a-/-) for functional studies.
  • Analysis of Toll-like receptor 4 (TLR4) signaling pathways and cytokine production.
  • Identification of HDM-derived ligands for Clec10a and Asgr1.

    • Main Results:

    • A stop-gain mutation in the Clec10a gene was identified in NC/Nga mice, correlating with HDM hypersensitivity.
    • CRISPR-Cas9 repair of the Clec10a mutation ameliorated HDM-induced dermatitis in NC/Nga mice.
    • Clec10a deficiency (Clec10a-/-) exacerbated HDM-induced dermatitis, indicating a protective role.
    • Clec10a on skin macrophages inhibits TLR4-mediated inflammation via its cytoplasmic motif.
    • Asialoglycoprotein receptor 1 (Asgr1) was identified as the human functional homolog of mouse Clec10a.
    • A mucin-like molecule in HDM acts as a ligand for both mouse Clec10a and human Asgr1.
    • Application of the HDM ligand reduced TLR4 ligand-induced dermatitis in mice.

    Conclusions:

    • The Clec10a mutation in NC/Nga mice is directly responsible for their hypersensitivity to HDM.
    • Clec10a plays a crucial role in maintaining skin homeostasis by suppressing inflammatory responses to HDM.
    • Human Asgr1 is a potential therapeutic target for managing HDM-induced allergic skin inflammation.
    • Targeting the Clec10a-ligand interaction offers a novel strategy for treating allergic dermatitis.