Evidence map›Paper›PMID 35113811›Full record

ArticleJCI insight2022

Dendritic cell immunoreceptor drives atopic dermatitis by modulating oxidized CaMKII-involved mast cell activation.

Xiaoyan Luo, Jingsi Chen, Huan Yang, Xinyue Hu, Martin P Alphonse, Yingchun Shen, Yuko Kawakami, Xiaoying Zhou, Wei Tu, Toshiaki Kawakami and 4 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. 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
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The C-type lectin receptor Dcir (Frontiers in immunology · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Xiaoyan LuoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jingsi ChenDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Huan YangDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Xinyue HuDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Martin P AlphonseDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yingchun ShenDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yuko KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
Xiaoying ZhouPediatric Dermatology, Children's Hospital, Chongqing Medical University, Chongqing, China.
Wei TuDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Toshiaki KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
Mei WanDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Nathan K ArcherDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Hua WangPediatric Dermatology, Children's Hospital, Chongqing Medical University, Chongqing, China.
Peisong GaoDivision of Allergy and Clinical Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USChildren's Hospital of Chongqing Medical University · CNLa Jolla Institute for Immunology · USCentral South University · CN

Funding

Environmental Pollutants Potentiate Allergic Inflammation via Functional Axis of Aryl hydrocarbon Receptor, ROS, and CaMKII in AsthmaR01AI141642 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2019 to 2024
$2.9M
Functional role of miR-511-3p in allergic asthma and its underlying mechanismsR01AI153331 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Peisong Gao · 2021 to 2026
$2.7M
Histamine-Releasing Factor Oligomers in Food AllergyR01AI146042 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2019 to 2022
$2.5M
IL-36 responses in Staphylococcus aureus driven skin inflammationR01AR073665 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2018 to 2022
$1.8M
STAT3-mediated immunity to Staphylococcus aureus in skinR01AR069502 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2016 to 2020
$1.8M
Crosstalk between FceRI and MAVS signaling pathways in mast cellsR21AI153867 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2020 to 2021
$503k
Regulation of allergen-induced mast cell activation and allergic inflammation through DCIRR21AI137547 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2018 to 2019
$450k
RhoA signaling controls mesenchymal stem cell lineage commitment via Lef-1 in asthmaR56AI143668 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2019 to 2019
$450k
Lineage Commitment of Mesenchymal Stem Cell in Allergen-induced Airway RemodelingR21AI109062 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2014 to 2015
$446k
NIAID NIH HHS R01 AI141642NIAID NIH HHS R01 AI146042NIAID NIH HHS R01 AI153331NIAID NIH HHS R21 AI109062NIAID NIH HHS R21 AI137547NIAID NIH HHS R21 AI153867NIAID NIH HHS R56 AI143668NIAMS NIH HHS R01 AR069502NIAMS NIH HHS R01 AR073665
6 · The paper itself

Abstract

Allergens have been identified as potential triggers in patients with atopic dermatitis (AD). Patients with AD are highly sensitive to cockroach allergen. The underlying mechanism, however, remains undetermined. Here, we established a cockroach allergen-induced AD-like mouse model, and we demonstrate that repeated exposure to cockroach allergen led to aggravated mouse skin inflammation, characterized by increased type 2 immunity, type 2 innate lymphoid cells (ILC2s), and mast cells. Increased mast cells were also observed in patients with AD. Mast cell-deficient mice (KitW-sh/W-sh) showed diminished skin inflammation, suggesting that mast cells are required in allergen-induced skin inflammation. Furthermore, DC immunoreceptor (DCIR) is upregulated in skin mast cells of patients with AD and mediates allergen binding and uptake. DCIR-/- mice or reconstituted KitW-sh/W-sh mice with DCIR-/- mast cells showed a significant reduction in AD-like inflammation. Both in vitro and in vivo analyses demonstrate that DCIR-/- mast cells had reduced IgE-mediated mast cell activation and passive cutaneous anaphylaxis. Mechanistically, DCIR regulates allergen-induced IgE-mediated mast cell ROS generation and oxidation of calmodulin kinase II (ox-CaMKII). ROS-resistant CaMKII (MM-VVδ) prevents allergen-induced mast cell activation and inflammatory mediator release. Our study reveals a DCIR/ROS/CaMKII axis that controls allergen-induced mast cell activation and AD-like inflammation.

Indexed as

CockroachesDermatitis, AtopicAllergensAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Dendritic CellsHumansImmunity, InnateImmunoglobulin EInflammationLectins, C-TypeLymphocytesMast CellsMiceReactive Oxygen SpeciesAllergensCalcium-Calmodulin-Dependent Protein Kinase Type 2Dcir protein, mouseImmunoglobulin ELectins, C-TypeReactive Oxygen SpeciesAllergyDermatologyImmunologyMouse modelsSkin

Identifiers

PMID35113811
PMCPMC8983143
OpenAlexW4210382938

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.