Evidence map›Paper›PMID 29943459›Full record

ArticleContact dermatitis2018

Regulation of contact sensitivity in non-obese diabetic (NOD) mice by innate immunity.

Marian Szczepanik, Monika Majewska-Szczepanik, Florence S Wong, Paulina Kowalczyk, Chandrashekhar Pasare, Li Wen

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Contact dermatitis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Exopolysaccharide Produced byMolecules (Basel, Switzerland) · 2019
    Article
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 4 institutions in 4 countries.

Marian SzczepanikDepartment of Internal Medicine, Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut.ORCID http://orcid.org/0000-0002-0388-2382
Monika Majewska-SzczepanikDepartment of Internal Medicine, Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut.
Florence S WongDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK.
Paulina KowalczykDepartment of Medical Biology, Health Science Faculty, Jagiellonian University Medical College, Krakow, Poland.
Chandrashekhar PasareDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas.
Li WenDepartment of Internal Medicine, Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut.ORCID http://orcid.org/0000-0002-8805-2934
Jagiellonian University · PLInstitute of Infection and Immunity · CAThe University of Texas Southwestern Medical Center · USYale University · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold, GERALD I SHULMAN · 1993 to 2026
$44.0M
Role of TLR9 in Beta Cell Function and DiabetesR01DK092882 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2012 to 2016
$1.8M
Dendritic cells in immuno-metabolic disorder in mouse and manR01DK100500 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2014 to 2017
$1.4M
Environment, innate immunity and type 1 diabetesR01DK088181 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2010 to 2013
$1.4M
Diabetes Mouse Core of DK P30-11-015National Science Center UMO-2012/05/B/NZ6/00997NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK088181NIDDK NIH HHS R01 DK092882NIDDK NIH HHS R01 DK100500NIH HHS DK092882DK100500
6 · The paper itself

Abstract

backgroundGenetic background influences allergic immune responses to environmental stimuli. Non-obese diabetic (NOD) mice are highly susceptible to environmental stimuli. Little is known about the interaction of autoimmune genetic factors with innate immunity in allergies, especially skin hypersensitivity.

objectivesTo study the interplay of innate immunity and autoimmune genetic factors in contact hypersensitivity (CHS) by using various innate immunity-deficient NOD mice.

methodsToll-like receptor (TLR) 2-deficient, TLR9-deficient and MyD88-deficient NOD mice were used to investigate CHS. The cellular mechanism was determined by flow cytometry in vitro and adoptive cell transfer in vivo. To investigate the role of MyD88 in dendritic cells (DCs) in CHS, we also used CD11c

resultsWe found that innate immunity negatively regulates CHS, as innate immunity-deficient NOD mice developed exacerbated CHS accompanied by increased numbers of skin-migrating CD11c

conclusionOur results suggest that the autoimmune-prone NOD genetic background aggravates CHS regulated by innate immunity, through DCs and T effector cells.

Indexed as

Adoptive TransferAnimalsB7-1 AntigenCell MovementCytokinesDendritic CellsDermatitis, ContactHistocompatibility Antigens Class IIImmunity, InnateLymph NodesMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutMyeloid Differentiation Factor 88Picryl ChlorideB7-1 AntigenCytokinesHistocompatibility Antigens Class IIMyd88 protein, mouseMyeloid Differentiation Factor 88Picryl ChlorideRNA, MessengerTlr2 protein, mouseTlr9 protein, mouseToll-Like Receptor 2Toll-Like Receptor 9contact sensitivitydendritic cellsnon-obese diabetic (NOD) mouseToll-like receptorTregs

Identifiers

PMID29943459
PMCPMC6126938
OpenAlexW2811064596

What OpenQuestion holds

Textmetadata
LicenceTDM
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.