Evidence map›Paper›PMID 30910955›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Enhanced oxidative phosphorylation in NKT cells is essential for their survival and function.

Ajay Kumar, Kalyani Pyaram, Emily L Yarosz, Hanna Hong, Costas A Lyssiotis, Shailendra Giri, Cheong-Hee Chang

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

80 citing papers in PubMed, 121 citations in OpenAlex.

  1. Lactylation Modification and Esophageal Cancer: Research Progress From Hypoxia-Induced Metabolic Reprogramming to Immune Escape.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  6. Human CD4Frontiers in immunology · 2026
    Article
  7. Metabolic control of innate-like T cells.Nature reviews. Immunology · 2026
    Review
  8. Frontiers in immunology · 2026
    Article
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20 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

7 authors at 2 institutions in 1 country.

Ajay KumarDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109.
Kalyani PyaramDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109.
Emily L YaroszImmunology Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109.
Hanna HongImmunology Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109.
Costas A LyssiotisDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109.
Shailendra GiriDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.ORCID 0000-0002-7123-829X
Cheong-Hee ChangDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109; heechang@umich.edu.
University of Michigan · USHenry Ford Health System · US

Funding

Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
Innate T cell metabolism and immune diseasesR01AI121156 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, CHEONG-HEE · 2016 to 2020
$1.9M
NIAID NIH HHS R01 AI121156NIDDK NIH HHS U24 DK097153
6 · The paper itself

Abstract

Cellular metabolism and signaling pathways are key regulators to determine conventional T cell fate and function, but little is understood about the role of cell metabolism for natural killer T (NKT) cell survival, proliferation, and function. We found that NKT cells operate distinct metabolic programming from CD4 T cells. NKT cells are less efficient in glucose uptake than CD4 T cells with or without activation. Gene-expression data revealed that, in NKT cells, glucose is preferentially metabolized by the pentose phosphate pathway and mitochondria, as opposed to being converted into lactate. In fact, glucose is essential for the effector functions of NKT cells and a high lactate environment is detrimental for NKT cell survival and proliferation. Increased glucose uptake and IFN-γ expression in NKT cells is inversely correlated with bacterial loads in response to bacterial infection, further supporting the significance of glucose metabolism for NKT cell function. We also found that promyelocytic leukemia zinc finger seemed to play a role in regulating NKT cells' glucose metabolism. Overall, our study reveals that NKT cells use distinct arms of glucose metabolism for their survival and function.

Indexed as

Cell ProliferationOxidative PhosphorylationAnimalsCD4-Positive T-LymphocytesCell SurvivalGlucoseMiceMice, KnockoutMitochondriaNatural Killer T-CellsPentose Phosphate PathwayPromyelocytic Leukemia Zinc Finger ProteinGlucosePromyelocytic Leukemia Zinc Finger ProteinZbtb16 protein, mouseglucoseNKTOXPHOSPLZF

Identifiers

PMID30910955
PMCPMC6462103
OpenAlexW2923756133

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.