Evidence map›Paper›PMID 37409131›Full record

ArticleFrontiers in immunology2023

MR1 deficiency enhances IL-17-mediated allergic contact dermatitis.

Naoya Imahashi, Masashi Satoh, Emanuela Clemente, Kazuhisa Yoshino, Mario Di Gioacchino, Kazuya Iwabuchi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 2 institutions in 2 countries.

Naoya ImahashiProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Masashi SatohProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Emanuela ClementeProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Kazuhisa YoshinoDepartment of Anesthesiology, School of Medicine, Kitasato University, Sagamihara, Japan.
Mario Di GioacchinoCenter for Advanced Studies and Technology (CAST), G. d'Annunzio University of Chieti-Pescara, Chiete, Italy.
Kazuya IwabuchiProgram in Cellular Immunology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Japan.
Kitasato University · JPUniversity of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major histocompatibility complex (MHC) class Ib molecules present antigens to subsets of T cells primarily involved in host defense against pathogenic microbes and influence the development of immune-mediated diseases. The MHC class Ib molecule MHC-related protein 1 (MR1) functions as a platform to select MR1-restricted T cells, including mucosal-associated invariant T (MAIT) cells in the thymus, and presents ligands to them in the periphery. MAIT cells constitute an innate-like T-cell subset that recognizes microbial vitamin B

Indexed as

Dermatitis, Allergic ContactHistocompatibility Antigens Class IInterleukin-17Minor Histocompatibility AntigensAnimalsDinitrofluorobenzeneMiceDinitrofluorobenzeneHistocompatibility Antigens Class IInterleukin-17Minor Histocompatibility AntigensMr1 protein, mouseallergydelayed-type hypersensitivitygamma/delta T cellsinnate T cellsneutrophils

Identifiers

PMID37409131
PMCPMC10319069
OpenAlexW4381334486

What Socratic 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 Socratic graph.