Evidence map›Paper›PMID 35833127›Full record

ArticleFrontiers in immunology2022

Th2 to Th1 Transition Is Required for Induction of Skin Lesions in an Inducible and Recurrent Murine Model of Cutaneous Lupus-Like Inflammation.

Nazgol-Sadat Haddadi, Purvi Mande, Tia Y Brodeur, Kaiyuan Hao, Grace E Ryan, Stephanie Moses, Sharon Subramanian, Xhuliana Picari, Khashayar Afshari, Ann Marshak-Rothstein and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Recent advances in cutaneous lupus.Journal of autoimmunity · 2022
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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

11 authors at 1 institution in 1 country.

Nazgol-Sadat HaddadiDepartment of Dermatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Purvi MandeDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Tia Y BrodeurDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Kaiyuan HaoDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Grace E RyanDepartment of Dermatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Stephanie MosesDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Sharon SubramanianDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Xhuliana PicariDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Khashayar AfshariDepartment of Dermatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Ann Marshak-RothsteinDepartment of Medicine, Division of Rheumatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
Jillian M RichmondDepartment of Dermatology, University of Massachusetts Chan Medical School, Worcester, MA, United States.
University of Massachusetts Chan Medical School · US

Funding

University of Massachusetts Center for Clinical Science and Translational SupplementUL1TR001453 · NCATS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUZURIAGA, KATHERINE F · 2015 to 2024
$39.0M
Innate Immunity Training ProgramT32AI095213 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SILVERMAN, NEAL · 2011 to 2025
$2.5M
Innate Immune activation of Cutaneous LupusR21AI136253 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 2018 to 2019
$461k
Mechanisms by which TLR9-deficiency and FasL Promote Cutaneous LupusR21AI145097 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 2019 to 2020
$461k
NCATS NIH HHS UL1 TR001453NIAID NIH HHS R21 AI136253NIAID NIH HHS R21 AI145097NIAID NIH HHS T32 AI095213
6 · The paper itself

Abstract

Cutaneous lupus erythematosus (CLE) is an autoimmune skin disease characterized by a strong IFN signature, normally associated with type I IFNs. However, increasing evidence points to an additional role for IFNγ, or at least a pathogenic T effector subset dependent on IFNγ, for disease progression. Nevertheless, Th2 effector subsets have also been implicated in CLE. We have now assessed the role of specific T cell subsets in the initiation and persistence of skin disease using a T cell-inducible murine model of CLE, dependent on KJ1-26 T cell recognition of an ovalbumin fusion protein. We found that only Th2-skewed cells, and not Th1-skewed cells, induced the development of skin lesions. However, we provide strong evidence that the Th2 disease-initiating cells convert to a more Th1-like functional phenotype

Indexed as

DermatitisLupus Erythematosus, CutaneousAnimalsDisease Models, AnimalInflammationInterferon Regulatory FactorsMiceTh1 CellsTh2 CellsInterferon Regulatory FactorsIrf5 protein, mouseCD4+ helper T cellcutaneous lupus erythematosusCXCR6Lupus flareTh1 & Th2

Identifiers

PMID35833127
PMCPMC9271959
OpenAlexW4283590960

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.