Evidence map›Paper›PMID 33535890›Full record

ArticleAutophagy2021

CD36 and LC3B initiated autophagy in B cells regulates the humoral immune response.

Chenfei He, Shan Wang, Chikai Zhou, Minghui He, Jin Wang, Marcus Ladds, Danai Lianoudaki, Saikiran K Sedimbi, David P Lane, Lisa S Westerberg and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  15. Lipid metabolism in B cell biology.Molecular oncology · 2024
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Fatty acid oxidation in immune function.Frontiers in immunology · 2024
    Review
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

12 authors at 2 institutions in 2 countries.

Chenfei HeDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-3373-8450
Shan WangDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-8471-5673
Chikai ZhouDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-9653-3466
Minghui HeDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Jin WangDepartment of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, P.R. China.
Marcus LaddsDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-9894-0169
Danai LianoudakiDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Saikiran K SedimbiDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-5243-8395
David P LaneDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Lisa S WesterbergDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Shuijie LiDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Mikael C I KarlssonDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Scavenger receptors are pattern recognition receptors that recognize both foreign and self-ligands, and initiate different mechanisms of cellular activation, often as co-receptors. The function of scavenger receptor CD36 in the immune system has mostly been studied in macrophages but it is also highly expressed by innate type B cells where its function is less explored. Here we report that CD36 is involved in macro-autophagy/autophagy in B cells, and in its absence, the humoral immune response is impaired. We found that CD36-deficient B cells exhibit a significantly reduced plasma cell formation, proliferation, mitochondrial mobilization and oxidative phosphorylation. These changes were accompanied by impaired initiation of autophagy, and we found that CD36 regulated autophagy and colocalized with autophagosome membrane protein MAP1LC3/LC3 (microtubule-associated protein 1 light chain 3). When we investigated T-cell-dependent immune responses, we found that mice with CD36 deficiency, specifically in B cells, exhibited attenuated germinal center responses, class switching, and antibody production as well as autophagosome formation. These findings establish a critical role for CD36 in B cell responses and may also contribute to our understanding of CD36-mediated autophagy in other cells as well as in B cell lymphomas that have been shown to express the receptor.

Indexed as

AutophagyImmunity, HumoralAnimalsAutophagosomesB-LymphocytesCD36 AntigensCell DifferentiationCell ProliferationHumansImmunoglobulin Class SwitchingMiceMicrotubule-Associated ProteinsPlasma CellsT-LymphocytesCD36 AntigensCD36 protein, humanMAP1LC3B protein, humanMicrotubule-Associated ProteinsAntibody responseautophagyb cellclass switchingscavenger receptors

Identifiers

PMID33535890
PMCPMC8632284
OpenAlexW3128062994

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.