Evidence map›Paper›PMID 29246800›Full record

ArticleThe Journal of investigative dermatology2018

Eosinophils Mediate Tissue Injury in the Autoimmune Skin Disease Bullous Pemphigoid.

Lan Lin, Bin-Jin Hwang, Donna A Culton, Ning Li, Susan Burette, Beverly H Koller, Kelly A Messingham, Janet A Fairley, James J Lee, Russell P Hall and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  6. Bullous pemphigoid.Nature reviews. Disease primers · 2025
    Review
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  8. Helicobacter pylori infection an underestimated trigger of bullous pemphigoid?Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025
    Article
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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

13 authors at 5 institutions in 2 countries.

Lan LinDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; School of Life Science and Biotechnology, Dalian University of Technology, Dalian, Liaoning, People's Republic of China.
Bin-Jin HwangDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Donna A CultonDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Ning LiDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Susan BuretteDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Beverly H KollerDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Kelly A MessinghamDepartment of Dermatology, University of Iowa, Iowa City, Iowa, USA.
Janet A FairleyDepartment of Dermatology, University of Iowa, Iowa City, Iowa, USA.
James J LeeMayo Clinic Arizona, Department of Biochemistry and Molecular Biology, Scottsdale, Arizona, USA.
Russell P HallDepartment of Dermatology, Duke University Medical Center, Durham, North Carolina, USA.
Lijia AnSchool of Life Science and Biotechnology, Dalian University of Technology, Dalian, Liaoning, People's Republic of China.
Luis A DiazDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Zhi LiuDepartment of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Electronic address: zhi_liu@med.unc.edu.
University of North Carolina at Chapel Hill · USUniversity of Iowa · USDalian University of Technology · CNDuke Medical Center · USMayo Clinic in Arizona · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
ETIOLOGY AND PATHOGENESIS OF PEMPHIGUSR01AR032599 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1987 to 2017
$5.2M
IMMUNOPATHOGENESIS OF BULLOUS PEMPHIGOIDR01AI040768 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2001 to 2016
$4.1M
PEMPHIGUS AND PEMPHIGOIDR01AR032081 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIAZ, LUIS A. · 1986 to 2011
$3.3M
Eosinophil-nerve Interactions in Mouse Models of DermatitisR01AR061567 · NIAMS · MAYO CLINIC ARIZONA · PI JACOBSEN, ELIZABETH A, JACOBY, DAVID B · 2012 to 2016
$2.9M
Innate Immunity in Bullous PemphigoidR01AI079240 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2010 to 2014
$1.8M
Role of the matrix metalloproteinase in pemphigus autoantibody-mediated epidermalR01AR061372 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, NING · 2012 to 2016
$1.5M
Genetic factors in IgE-mediated food allergiesR21AI088628 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KOLLER, BEVERLY H · 2010 to 2011
$405k
IMMUNOPATHOGENESIS OF BULLOUS PEMPHIGOIDR29AI040768 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 1996 to 2000
$101k
NCI NIH HHS P30 CA016086NIAID NIH HHS R01 AI040768NIAID NIH HHS R01 AI079240NIAID NIH HHS R21 AI088628NIAID NIH HHS R29 AI040768NIAMS NIH HHS R01 AR032081NIAMS NIH HHS R01 AR032599NIAMS NIH HHS R01 AR061372NIAMS NIH HHS R01 AR061567
6 · The paper itself

Abstract

Eosinophils are typically associated with unique inflammatory settings, including allergic inflammation and helminth infections. However, new information suggests that eosinophils contribute more broadly to inflammatory responses and participate in local immune regulation and the tissue remodeling/repair events linked with a variety of diseases. Eosinophilic infiltration has long been a histologic hallmark of bullous pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantibodies directed against basement membrane protein BP180. However, the exact role of eosinophils in disease pathogenesis remains largely unknown. We show here that eosinophils are necessary for IgE autoantibody-mediated BP blister formation in a humanized IgE receptor mouse model of BP. Disease severity is IgE dose dependent and correlates with the degree of eosinophil infiltration in the skin. Furthermore, IgE autoantibodies fail to induce BP in eosinophil-deficient mice, confirming that eosinophils are required for IgE-mediated tissue injury. Thus, eosinophils provide the cellular link between IgE autoantibodies and skin blistering in this murine model of BP. These findings suggest a role for eosinophils in autoimmune disease and have important implications for the treatment of BP and other antibody-mediated inflammatory and autoimmune diseases.

Indexed as

Acute DiseaseAnimalsAutoantibodiesAutoantigensCollagen Type XVIIEosinophilsHumansImmunoglobulin EMiceNeutrophilsNon-Fibrillar CollagensPemphigoid, BullousAutoantibodiesAutoantigensCollagen Type XVIIImmunoglobulin ENon-Fibrillar Collagens

Identifiers

PMID29246800
PMCPMC7531612
OpenAlexW2772852367

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.