Evidence map›Paper›PMID 29326381›Full record

ArticleThe Journal of experimental medicine2018

B1a B cells require autophagy for metabolic homeostasis and self-renewal.

Alexander J Clarke, Thomas Riffelmacher, Daniel Braas, Richard J Cornall, Anna Katharina Simon

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
9.9field-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.

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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. A guide to B cell metabolism.Nature reviews. Immunology · 2026
    Review
  4. Review
  5. Review
  6. B1 Cells for Life.Immunological reviews · 2026
    Review
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  9. Review
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41 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 2 institutions in 2 countries.

Alexander J ClarkeKennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK alexander.clarke@kennedy.ox.ac.uk.ORCID 0000-0003-2846-7860
Thomas RiffelmacherKennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK.ORCID 0000-0002-0372-5272
Daniel BraasDepartment of Molecular and Medical Pharmacology and UCLA Metabolomics Center, University of California, Los Angeles, Los Angeles, CA.
Richard J CornallNuffield Department of Medicine, Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK.
Anna Katharina SimonKennedy Institute of Rheumatology and Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, England, UK katja.simon@kennedy.ox.ac.uk.ORCID 0000-0002-4077-7995
University of Oxford · GBUniversity of California, Los Angeles · US

Funding

Medical Research Council MC_UU_00008/6Medical Research Council MC_UU_12010/6Wellcome TrustWellcome Trust 103830/Z/14/ZWellcome Trust 104549/Z/14/Z
6 · The paper itself

Abstract

Specific metabolic programs are activated by immune cells to fulfill their functional roles, which include adaptations to their microenvironment. B1 B cells are tissue-resident, innate-like B cells. They have many distinct properties, such as the capacity to self-renew and the ability to rapidly respond to a limited repertoire of epitopes. The metabolic pathways that support these functions are unknown. We show that B1 B cells are bioenergetically more active than B2 B cells, with higher rates of glycolysis and oxidative phosphorylation, and depend on glycolysis. They acquire exogenous fatty acids and store lipids in droplet form. Autophagy is differentially activated in B1a B cells, and deletion of the autophagy gene

Indexed as

AnimalsAutophagyAutophagy-Related Protein 7B-Lymphocyte SubsetsCell LineageCell Self RenewalCell SurvivalFatty AcidsFemaleGlycolysisHomeostasisLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutAtg7 protein, mouseAutophagy-Related Protein 7Fatty Acids

Identifiers

PMID29326381
PMCPMC5789411
OpenAlexW2951598355

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.