Evidence map›Paper›PMID 12531880›Full record

ArticleThe Journal of clinical investigation2003

Leptin surge precedes onset of autoimmune encephalomyelitis and correlates with development of pathogenic T cell responses.

Veronica Sanna, Antonio Di Giacomo, Antonio La Cava, Robert I Lechler, Silvia Fontana, Serafino Zappacosta, Giuseppe Matarese

Registry-linked trialOpen access · greenAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04042415 (Calorie Restriction as a Novel Therapeutic Tool to Manipulate Immunity and Improve Therapeutic Potential of First Line Drug Treatments During Relapsing Remitting Multiple Sclerosis), which is not on this map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
7.9field-weighted citation impact, top 1% 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.

NCT04042415 naactive not recruitingnot on this mapstarted 2020, after this paper: background citation

Calorie Restriction as a Novel Therapeutic Tool to Manipulate Immunity and Improve Therapeutic Potential of First Line Drug Treatments During Relapsing Remitting Multiple Sclerosis

TypeinterventionalSponsorFederico II UniversityRan2020 to 2025Enrolled93ConditionsMultiple Sclerosis, Relapsing-Remitting, Caloric RestrictionArmsCaloric restriction, Caloric restriction without cow's milk and gluten
3 · Its place in the literature

Who cites it

112 citing papers in PubMed, 310 citations in OpenAlex.

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  14. The Role of Adipokines in the Pathologies of the Central Nervous System.International journal of molecular sciences · 2023
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52 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 3 countries.

Veronica SannaGruppo di ImmunoEndocrinologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche (IEOS-CNR), Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II, Napoli, Italy.
Antonio Di Giacomo
Antonio La Cava
Robert I Lechler
Silvia Fontana
Serafino Zappacosta
Giuseppe Matarese
University of Naples Federico II · ITCellular Research (United States) · USImperial College London · GBMultiMedica · ITUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the work presented here, we explored the influence of leptin on the kinetics of experimental autoimmune encephalomyelitis (EAE) onset, in the EAE-associated inflammatory anorexia, and in the development of pathogenic T cell responses. We found that the expression of serum leptin increased before the clinical onset of EAE in disease-susceptible C57BL/6J (H-2(b)) and SJL/J (H-2(s)) strains of mice, which are models of chronic-progressive and relapsing-remitting EAE, respectively. This increase in serum leptin correlated with disease susceptibility, reduction in food intake, and decrease in body weight. Indeed, acute starvation, which is able to prevent the increase in serum leptin, delayed disease onset and attenuated clinical symptoms by inducing a T helper 2 cytokine switch. Furthermore, immunohistochemical analysis revealed a parallel in situ production of leptin in inflammatory infiltrates and in neurons only during the acute/active phase of both chronic-progressive and relapsing-remitting EAE. We also found that leptin secretion by activated T cells sustained their proliferation in an autocrine loop, since antileptin receptor antibodies were able to inhibit the proliferative response of autoreactive T cells in vitro. Given that leptin appears to regulate EAE susceptibility, inflammatory anorexia, and pathogenic T-cell immune function, we postulate that it may offer a potential target in the treatment of multiple sclerosis.

Indexed as

AnimalsAnorexiaDisease SusceptibilityEncephalomyelitis, Autoimmune, ExperimentalFemaleLeptinLymphocyte ActivationMaleMiceMice, Inbred C57BLTh1 CellsWeight LossLeptin

Identifiers

PMID12531880
PMCPMC151876
OpenAlexW2106709031

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.