Evidence map›Paper›PMID 31363227›Full record

ReviewNature reviews. Drug discovery2019

Targeting metabolism to regulate immune responses in autoimmunity and cancer.

Chirag H Patel, Robert D Leone, Maureen R Horton, Jonathan D Powell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

167 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. International journal of molecular sciences · 2026
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107 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

4 authors.

Chirag H PatelBloomberg~Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Robert D LeoneBloomberg~Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Maureen R HortonDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jonathan D PowellBloomberg~Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. poweljo@jhmi.edu.ORCID http://orcid.org/0000-0002-0850-2852

Funding

PATHOPHYSIOLOGY OF MYOCARDIAL DISEASEST32HL007227 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Chulan Kwon, WENDY S POST · 1985 to 2026
$21.2M
CELLULAR &MOLECULAR MECH OF INFLAMMATORY REACTIONST32AI007247 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Joel L Pomerantz · 1985 to 2026
$10.2M
A central role for mTOR in Determining T Cell Activation versus ToleranceR01AI077610 · NIAID · JOHNS HOPKINS UNIVERSITY · PI POWELL, JONATHAN D · 2009 to 2019
$4.0M
Cell-targeted glutamine antagonists as a novel therapy for lymphomaR01CA229451 · NCI · JOHNS HOPKINS UNIVERSITY · PI SLUSHER, BARBARA STAUCH · 2018 to 2022
$2.3M
Targeting Tumor Metabolism as a Means of Enhancing ImmunotherapyR01CA226765 · NCI · JOHNS HOPKINS UNIVERSITY · PI LEONE, ROBERT DAVID · 2019 to 2023
$1.9M
Immunotherapy induced Trm arrest and reverse lung fibrosisR01HL141490 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HILLEL, ALEXANDER · 2018 to 2021
$1.6M
NCI NIH HHS R01 CA226765NCI NIH HHS R01 CA229451NHLBI NIH HHS R01 HL141490NHLBI NIH HHS T32 HL007227NIAID NIH HHS R01 AI077610NIAID NIH HHS T32 AI007247
6 · The paper itself

Abstract

Metabolic programming is emerging as a critical mechanism to alter immune cell activation, differentiation and function. Targeting metabolism does not completely suppress or activate the immune system but selectively regulates immune responses. The different metabolic requirements of the diverse cells that constitute an immune response provide a unique opportunity to separate effector functions from regulatory functions. Likewise, cells can be metabolically reprogrammed to promote either their short-term effector functions or long-term memory capacity. Studies in the growing field of immunometabolism support a paradigm of 'cellular selectivity based on demand', in which generic inhibitors of ubiquitous metabolic processes selectively affect cells with the greatest metabolic demand and have few effects on other cells of the body. Targeting metabolism, rather than particular cell types or cytokines, in metabolically demanding processes such as autoimmunity, graft rejection, cancer and uncontrolled inflammation could lead to successful strategies in controlling the pathogenesis of these complex disorders.

Indexed as

Autoimmune DiseasesAutoimmunityGraft RejectionHumansImmune SystemImmunomodulationInflammationMetabolismModels, BiologicalNeoplasms

Identifiers

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.