Evidence map›Paper›PMID 27588900›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Leptin promotes systemic lupus erythematosus by increasing autoantibody production and inhibiting immune regulation.

Elaine V Lourenço, Aijing Liu, Giuseppe Matarese, Antonio La Cava

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.8field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  12. Leptin signaling and leptin resistance.Medical review (2021) · 2022
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  19. An Update on the Role of Leptin in the Immuno-Metabolism of Cartilage.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Elaine V LourençoDepartment of Medicine, University of California, Los Angeles, CA 90095;
Aijing LiuDepartment of Medicine, University of California, Los Angeles, CA 90095;
Giuseppe MatareseDipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli Federico II, 80131 Naples, Italy; Istituto di Endocrinologia e Oncologia Sperimentale-Consiglio Nazionale delle Ricerche, 80131 Naples, Italy.ORCID 0000-0001-9429-0616
Antonio La CavaDepartment of Medicine, University of California, Los Angeles, CA 90095; ALaCava@mednet.ucla.edu.
University of California, Los Angeles · USInstitute for Experimental Endocrinology and Oncology · IT

Funding

Role of Leptin in Systemic Lupus ErythematosusR01AR053239 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LA CAVA, ANTONIO · 2006 to 2010
$1.6M
Leptin and mTOR: metabolic partners in autoimmunityR21AI109677 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LA CAVA, ANTONIO · 2015 to 2016
$424k
European Research Council 310496NIAID NIH HHS R21 AI109677NIAMS NIH HHS R01 AR053239
6 · The paper itself

Abstract

Leptin is an adipocytokine that plays a key role in the modulation of immune responses and the development and maintenance of inflammation. Circulating levels of leptin are elevated in systemic lupus erythematosus (SLE) patients, but it is not clear whether this association can reflect a direct influence of leptin on the propathogenic events that lead to SLE. To investigate this possibility, we compared the extent of susceptibility to SLE and lupus manifestations between leptin-deficient (ob/ob) and H2-matched leptin-sufficient (wild-type, WT) mice that had been treated with the lupus-inducing agent pristane. Leptin deficiency protected ob/ob mice from the development of autoantibodies and renal disease and increased the frequency of immunoregulatory T cells (Tregs) compared with leptin-sufficient WT mice. The role of leptin in the development of SLE was confirmed in the New Zealand Black (NZB) × New Zealand White (NZW)F1 (NZB/W) mouse model of spontaneous SLE, where elevated leptin levels correlated with disease manifestations and the administration of leptin accelerated development of autoantibodies and renal disease. Conversely, leptin antagonism delayed disease progression and increased survival of severely nephritic NZB/W mice. At the cellular level, leptin promoted effector T-cell responses and facilitated the presentation of self-antigens to T cells, whereas it inhibited the activity of regulatory CD4 T cells. The understanding of the role of leptin in modulating autoimmune responses in SLE can open possibilities of leptin-targeted therapeutic intervention in the disease.

Indexed as

AnimalsAutoantibodiesAutoimmunityDisease Models, AnimalHumansImmunity, InnateInflammationLeptinLupus Erythematosus, SystemicMiceMice, Inbred NZBTerpenesT-Lymphocytes, RegulatoryAutoantibodiesLeptinpristaneTerpenesanimal modelsautoimmunityimmune regulationleptinsystemic lupus erythematosus

Identifiers

PMID27588900
PMCPMC5035847
OpenAlexW2510024185

What OpenQuestion holds

Textmetadata
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.