Evidence map›Paper›PMID 24043888›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis.

Ruobing Wang, Bao Lu, Craig Gerard, Norma P Gerard

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Non-heat inactivated autologous serum increases accuracy of in vitro CFSE lymphocyte proliferation test (LPT) for nickel.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020
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  14. T Cell Expression of C5a Receptor 2 Augments Murine Regulatory T Cell (TJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
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  16. Review
  17. C5L2, the Second C5a Anaphylatoxin Receptor, Suppresses LPS-Induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2016
    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

4 authors at 2 institutions in 1 country.

Ruobing WangIna Sue Perlmutter Laboratory, Division of Respiratory Diseases, Department of Pediatrics, Children's Hospital, Boston, MA 02115;
Bao Lu
Craig Gerard
Norma P Gerard
Boston Children's Hospital · USHarvard University · US

Funding

ASTHMA, AIRWAY INFLAMMATION AND BETA CHEMOKINE RECEPTORSR01AI039759 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GERARD, CRAIG · 1996 to 2013
$4.1M
MOLECULAR PATHOLOGY OF CHRONIC LUNG DISEASER01HL051366 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI GERARD, CRAIG · 1994 to 2013
$3.9M
NHLBI NIH HHS HL051366NHLBI NIH HHS R01 HL051366NIAID NIH HHS AI039759NIAID NIH HHS R01 AI039759
6 · The paper itself

Abstract

The complement anaphylatoxin C5a is a critical mediator of allergic contact dermatitis, bridging essential aspects of innate and adaptive immunity. This anaphylatoxin functions by interacting with two 7-transmembrane segment receptors, the C5aR and C5L2. The C5aR is a classical G protein coupled receptor, whereas C5L2 is deficient in coupling to G proteins because of variations in the sequence. Our previous work in human neutrophils revealed a unique role for C5L2 in negatively modulating anaphylatoxin receptor mediated cellular activation through interactions with β-arrestin. When C5L2 is deficient, C5aR-mediated β-arrestin signaling is greatly enhanced. The work described in this study was undertaken first to determine the effect of C5L2 deficiency in a murine model of contact sensitivity, and second to determine whether the resultant exacerbation of inflammatory parameters reflects a negative modulatory function of C5L2 on the C5aR. First, we find dramatic increases in inflammation in C5L2(-/-) animals compared with wild type mice. Second, these increases are completely reversed following administration of mAb against the C5aR. Thus, in allergic contact sensitivity, as in isolated human neutrophils, C5L2 functions to suppress C5a-C5aR-mediated responses, further underscoring its role as a negative regulator of anaphylatoxin activity.

Indexed as

AnimalsAntibodies, MonoclonalArrestinsbeta-ArrestinsComplement C5aDermatitis, Allergic ContactFemaleInflammationLymph NodesMiceMice, Inbred BALB CMice, KnockoutReceptor, Anaphylatoxin C5aReceptors, ChemokineSignal TransductionAntibodies, MonoclonalArrestinsbeta-ArrestinsC5ar2 protein, mouseComplement C5aReceptor, Anaphylatoxin C5aReceptors, Chemokine

Identifiers

PMID24043888
PMCPMC4551435
OpenAlexW2142636652

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.