Evidence map›Paper›PMID 19890385›Full record

ArticlePloS one2009

Mechanism of dinitrochlorobenzene-induced dermatitis in mice: role of specific antibodies in pathogenesis.

Elizabeth Yan Zhang, Aaron Yun Chen, Bao Ting Zhu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 78 citations in OpenAlex.

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  15. Salvianolic Acid A Suppresses DNCB-Induced Atopic Dermatitis-Like Symptoms in BALB/c Mice.Evidence-based complementary and alternative medicine : eCAM · 2021
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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

3 authors at 1 institution in 1 country.

Elizabeth Yan ZhangDepartment of Pharmacology, Toxicology and Therapeutics, School of Medicine, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Aaron Yun Chen
Bao Ting Zhu
University of Kansas Medical Center · US

Funding

THE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2006 to 2011
$12.1M
2-METHOXYESTRADIOL &HORMONAL CANCERR01CA097109 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ZHU, BAO-TING · 2003 to 2006
$826k
Selective Induction of Estrogen Conjugative MetabolismR01CA092391 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ZHU, BAO-TING · 2003 to 2006
$826k
NCI NIH HHS CA92391NCI NIH HHS CA97109NCI NIH HHS R01 CA092391NCI NIH HHS R01 CA097109NCRR NIH HHS P20 RR021940NCRR NIH HHS P20RR021940
6 · The paper itself

Abstract

backgroundDinitrochlorobenzene-induced contact hypersensitivity is widely considered as a cell-mediated rather than antibody-mediated immune response. At present, very little is known about the role of antigen-specific antibodies and B cells in the development of dinitrochlorobenzene-induced hypersensitivity reactions, and this is the subject of the present investigation. METHODOLOGY/PRINCIPAL

findingsData obtained from multiple lines of experiments unequivocally showed that the formation of dinitrochlorobenzene-specific Abs played an important role in the development of dinitrochlorobenzene-induced contact hypersensitivity. The appearance of dinitrochlorobenzene-induced skin dermatitis matched in timing the appearance of the circulating dinitrochlorobenzene-specific antibodies. Adoptive transfer of sera containing dinitrochlorobenzene-specific antibodies from dinitrochlorobenzene-treated mice elicited a much stronger hypersensitivity reaction than the adoptive transfer of lymphocytes from the same donors. Moreover, dinitrochlorobenzene-induced contact hypersensitivity was strongly suppressed in B cell-deficient mice with no DNCB-specific antibodies. It was also observed that treatment of animals with dinitrochlorobenzene polarized Th cells into Th2 differentiation by increasing the production of Th2 cytokines while decreasing the production of Th1 cytokines. CONCLUSIONS/SIGNIFICANCE: In striking contrast to the long-held belief that dinitrochlorobenzene-induced contact hypersensitivity is a cell-mediated immune response, the results of our present study demonstrated that the production of dinitrochlorobenzene-specific antibodies by activated B cells played an indispensible role in the pathogenesis of dinitrochlorobenzene-induced CHS. These findings may provide new possibilities in the treatment of human contact hypersensitivity conditions.

Indexed as

AnimalsAntibodiesB-LymphocytesCell DifferentiationCytokinesDermatitis, Allergic ContactDinitrochlorobenzeneFemaleImmunity, CellularIrritantsMaleMiceMice, Inbred C57BLMice, Inbred ICRSkinTh1 CellsAntibodiesCytokinesDinitrochlorobenzeneIrritants

Identifiers

PMID19890385
PMCPMC2766640
OpenAlexW2043287196

What OpenQuestion holds

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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.