Evidence map›Paper›PMID 26586568›Full record

ArticleCell death and differentiation2016

Autophagy is dispensable for B-cell development but essential for humoral autoimmune responses.

J Arnold, D Murera, F Arbogast, J-D Fauny, S Muller, F Gros

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
9.2field-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

77 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. A guide to B cell metabolism.Nature reviews. Immunology · 2026
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17 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

6 authors at 3 institutions in 1 country.

J ArnoldCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
D MureraCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
F ArbogastCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
J-D FaunyCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
S MullerCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
F GrosCNRS, Immunopathology and Therapeutic Chemistry/Laboratory of Excellence MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Institut de Biologie Moléculaire et Cellulaire · FRImmunologie, Immunopathologie et Chimie Thérapeutique · FRUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To gain new insight into the role of B-cell autophagy, we generated two novel mouse models deficient for the autophagy-related gene (Atg)5, one from the outset pro-B cell stage (Atg5(f/-) Mb1 cre) and the other in mature B cells only (Atg5(f/-) CD21 cre). We show that autophagy is dispensable for pro- to pre-B cell transition, but necessary at a basal level to maintain normal numbers of peripheral B cells. It appears non-essential for B-cell activation under B-cell receptor stimulation but required for their survival after lipopolysaccharide stimulation that drives plasmablast differentiation and for specific IgM production after immunization. Results obtained using Atg5(f/-) CD21 cre × C57BL/6(lpr/lpr) autoimmune-prone mice show that B-cell autophagy is involved in the maintenance of anti-nuclear antibody secretion, elevated number of long-lived plasma cells, and sustains IgG deposits in the kidneys. Thus, treatments specifically targeting autophagy might be beneficial in systemic autoimmune diseases.

Indexed as

AnimalsAutoimmunityAutophagyB-LymphocytesCells, CulturedMiceMice, Inbred C57BL

Identifiers

PMID26586568
PMCPMC4832104
OpenAlexW2219755458

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.