Evidence map›Paper›PMID 25401752›Full record

ArticlePloS one2014

Leptin enhances availability of apoptotic cell-derived self-antigen in systemic lupus erythematosus.

Gil Amarilyo, Noriko Iikuni, Aijing Liu, Giuseppe Matarese, Antonio La Cava

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Leptin: an unappreciated key player in SLE.Clinical rheumatology · 2020
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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

5 authors at 2 institutions in 2 countries.

Gil AmarilyoUniversity of California Los Angeles, California, Los Angeles, United States of America.
Noriko IikuniUniversity of California Los Angeles, California, Los Angeles, United States of America.
Aijing LiuUniversity of California Los Angeles, California, Los Angeles, United States of America.
Giuseppe MatareseUniversità di Salerno, Baronissi, Italy; IRCCS MultiMedica, Milan, Italy.
Antonio La CavaUniversity of California Los Angeles, California, Los Angeles, United States of America.
University of California, Los Angeles · USMultiMedica · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In systemic lupus erythematosus (SLE), the availability of self-antigen promotes and fuels self-reactive immune responses. Apoptotic cells represent a major source of self-antigens, and an impairment of the removal of apoptotic material containing self-antigen can contribute to the development of autoimmunity. To address whether the adipocytokine leptin--which favors autoimmune responses through little understood mechanisms--could modulate the handling of apoptotic cells in SLE, we evaluated the ability of leptin to modulate the capacity of macrophages to phagocytose apoptotic bodies in (NZB × NZW)F1 lupus mice. It was found that leptin promoted phagocytosis of apoptotic cells by macrophages by modulating cAMP levels in macrophages. This finding associated with an increased availability of antigen that favored the development of T cell responses to apoptotic-derived antigen. As leptin promotes macrophage phagocytosis of apoptotic bodies in SLE and subsequent availability of apoptotic-derived antigen to T cells, an inhibition of this process via leptin blockade might have a therapeutic potential in SLE.

Indexed as

ApoptosisAnimalsAutoantigensAutoimmunityCell LineCyclic AMPDisease Models, AnimalFemaleLeptinLupus Erythematosus, SystemicLymphocyte ActivationMacrophagesMiceMice, TransgenicPhagocytosisT-LymphocytesAutoantigensCyclic AMPLeptin

Identifiers

PMID25401752
PMCPMC4234630
OpenAlexW2045133770

What Socratic 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 Socratic graph.