Evidence map›Paper›PMID 23690440›Full record

ArticleThe Journal of experimental medicine2013

Lymphoid tissue phospholipase A2 group IID resolves contact hypersensitivity by driving antiinflammatory lipid mediators.

Yoshimi Miki, Kei Yamamoto, Yoshitaka Taketomi, Hiroyasu Sato, Kanako Shimo, Tetsuyuki Kobayashi, Yukio Ishikawa, Toshiharu Ishii, Hiroki Nakanishi, Kazutaka Ikeda and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
10.0field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 129 citations in OpenAlex.

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  17. The Roles of sPLABiomolecules · 2023
    Review
  18. Article
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17 more citing papers are in PubMed but not listed here.

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

19 authors at 11 institutions in 3 countries.

Yoshimi MikiLipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Kei Yamamoto
Yoshitaka Taketomi
Hiroyasu Sato
Kanako Shimo
Tetsuyuki Kobayashi
Yukio Ishikawa
Toshiharu Ishii
Hiroki Nakanishi
Kazutaka Ikeda
Ryo Taguchi
Kenji Kabashima
Makoto Arita
Hiroyuki Arai
Gérard Lambeau
James M Bollinger
Shuntaro Hara
Michael H Gelb
Makoto Murakami
Tokyo Metropolitan Institute of Medical Science · JPShowa University · JPToho University · JPUniversity of Tokyo Health Sciences · JPUniversity of Washington · USAkita University · JPChubu University · JPInstitut de Pharmacologie Moléculaire et Cellulaire · FRKeio University · JPKyoto University · JPOchanomizu University · JP

Funding

Biochemical Studies of 14-kDa Phospholipases A2R37HL036235 · NHLBI · UNIVERSITY OF WASHINGTON · PI GELB, MICHAEL H · 2007 to 2016
$4.1M
NHLBI NIH HHS R37 HL036235
6 · The paper itself

Abstract

Resolution of inflammation is an active process that is mediated in part by antiinflammatory lipid mediators. Although phospholipase A2 (PLA2) enzymes have been implicated in the promotion of inflammation through mobilizing lipid mediators, the molecular entity of PLA2 subtypes acting upstream of antiinflammatory lipid mediators remains unknown. Herein, we show that secreted PLA2 group IID (PLA2G2D) is preferentially expressed in CD11c(+) dendritic cells (DCs) and macrophages and displays a pro-resolving function. In hapten-induced contact dermatitis, resolution, not propagation, of inflammation was compromised in skin and LNs of PLA2G2D-deficient mice (Pla2g2d(-/-)), in which the immune balance was shifted toward a proinflammatory state over an antiinflammatory state. Bone marrow-derived DCs from Pla2g2d(-/-) mice were hyperactivated and elicited skin inflammation after intravenous transfer into mice. Lipidomics analysis revealed that PLA2G2D in the LNs contributed to mobilization of a pool of polyunsaturated fatty acids that could serve as precursors for antiinflammatory/pro-resolving lipid mediators such as resolvin D1 and 15-deoxy-Δ(12,14)-prostaglandin J2, which reduced Th1 cytokine production and surface MHC class II expression in LN cells or DCs. Altogether, our results highlight PLA2G2D as a "resolving sPLA2" that ameliorates inflammation through mobilizing pro-resolving lipid mediators and points to a potential use of this enzyme for treatment of inflammatory disorders.

Indexed as

AnimalsAnti-Inflammatory AgentsDendritic CellsDermatitis, ContactFatty Acids, UnsaturatedGroup II Phospholipases A2HumansImmunologic FactorsInflammationLipidsLymphoid TissueMacrophagesMaleMiceMice, Inbred C57BLMice, TransgenicAnti-Inflammatory AgentsFatty Acids, UnsaturatedGroup II Phospholipases A2Immunologic FactorsLipidsphosphatidylethanolaminePhosphatidylethanolaminesPla2g2d protein, mouse

Identifiers

PMID23690440
PMCPMC3674707
OpenAlexW2159466612

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.