Evidence map›Paper›PMID 24273001›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Leptin metabolically licenses T cells for activation to link nutrition and immunity.

Donte C Saucillo, Valerie A Gerriets, John Sheng, Jeffrey C Rathmell, Nancie J Maciver

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

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 5 pooled it
6.3field-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

170 citing papers in PubMed, 5 syntheses or guidelines pooled it, 292 citations in OpenAlex.

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  18. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
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110 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

5 authors at 3 institutions in 1 country.

Donte C SaucilloDivision of Pediatric Endocrinology and Diabetes, Duke University Medical Center, Durham, NC 27710;
Valerie A Gerriets
John Sheng
Jeffrey C Rathmell
Nancie J Maciver
Duke University Hospital · USDuke Medical Center · USDuke University · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 1985 to 2026
$174.8M
T cell metabolism as a determinant of differentiation in allergic asthmaR01HL108006 · NHLBI · VANDERBILT UNIVERSITY · PI RATHMELL, JEFFREY C. · 2011 to 2014
$1.5M
Leptin as a Regulator of T Cell Metabolism and FunctionK08DK087944 · NIDDK · DUKE UNIVERSITY · PI MACIVER, NANCIE · 2010 to 2014
$678k
NCI NIH HHS P30 CA014236NHLBI NIH HHS R01 HL108006NHLBI NIH HHS R01-HL108006NIDDK NIH HHS K08 DK087944NIDDK NIH HHS K08-DK087944
6 · The paper itself

Abstract

Immune responses are highly energy-dependent processes. Activated T cells increase glucose uptake and aerobic glycolysis to survive and function. Malnutrition and starvation limit nutrients and are associated with immune deficiency and increased susceptibility to infection. Although it is clear that immunity is suppressed in times of nutrient stress, mechanisms that link systemic nutrition to T cell function are poorly understood. We show in this study that fasting leads to persistent defects in T cell activation and metabolism, as T cells from fasted animals had low glucose uptake and decreased ability to produce inflammatory cytokines, even when stimulated in nutrient-rich media. To explore the mechanism of this long-lasting T cell metabolic defect, we examined leptin, an adipokine reduced in fasting that regulates systemic metabolism and promotes effector T cell function. We show that leptin is essential for activated T cells to upregulate glucose uptake and metabolism. This effect was cell intrinsic and specific to activated effector T cells, as naive T cells and regulatory T cells did not require leptin for metabolic regulation. Importantly, either leptin addition to cultured T cells from fasted animals or leptin injections to fasting animals was sufficient to rescue both T cell metabolic and functional defects. Leptin-mediated metabolic regulation was critical, as transgenic expression of the glucose transporter Glut1 rescued cytokine production of T cells from fasted mice. Together, these data demonstrate that induction of T cell metabolism upon activation is dependent on systemic nutritional status, and leptin links adipocytes to metabolically license activated T cells in states of nutritional sufficiency.

Indexed as

AnimalsCytokinesFastingGlucoseGlucose Transporter Type 1GlycolysisInflammation MediatorsLeptinLymphocyte ActivationMiceMice, KnockoutMitochondriaReceptors, LeptinT-Lymphocyte SubsetsCytokinesGlucoseGlucose Transporter Type 1Inflammation MediatorsLeptinReceptors, Leptin

Identifiers

PMID24273001
PMCPMC3872216
OpenAlexW2117971406

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.