Evidence map›Paper›PMID 30319621›Full record

ArticleFrontiers in immunology2018

The Mitochondrion-lysosome Axis in Adaptive and Innate Immunity: Effect of Lupus Regulator Peptide P140 on Mitochondria Autophagy and NETosis.

Mykolas Bendorius, Indira Neeli, Fengjuan Wang, Srinivasa Reddy Bonam, Eszter Dombi, Nelly Buron, Annie Borgne-Sanchez, Joanna Poulton, Marko Radic, Sylviane Muller

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Therapeutic effects of peptide P140 in a mouse periodontitis model.Cellular and molecular life sciences : CMLS · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Lysosomes as a therapeutic target.Nature reviews. Drug discovery · 2019
    Review
  14. 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

10 authors at 4 institutions in 3 countries.

Mykolas BendoriusUnit Biotechnology and Cell Signaling, Laboratory of Excellence Medalis, CNRS, Strasbourg University, Illkirch, France.
Indira NeeliDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Fengjuan WangUnit Biotechnology and Cell Signaling, Laboratory of Excellence Medalis, CNRS, Strasbourg University, Illkirch, France.
Srinivasa Reddy BonamUnit Biotechnology and Cell Signaling, Laboratory of Excellence Medalis, CNRS, Strasbourg University, Illkirch, France.
Eszter DombiNuffield Department of Women's and Reproductive Health, Women's Centre, Oxford, United Kingdom.
Nelly BuronMitologics SAS, Paris, France.
Annie Borgne-SanchezMitologics SAS, Paris, France.
Joanna PoultonNuffield Department of Women's and Reproductive Health, Women's Centre, Oxford, United Kingdom.
Marko RadicDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Sylviane MullerUnit Biotechnology and Cell Signaling, Laboratory of Excellence Medalis, CNRS, Strasbourg University, Illkirch, France.
Biotechnologie et Signalisation Cellulaire · FRNuffield Health · GBUniversity of Tennessee Health Science Center · USCentre National de la Recherche Scientifique · FR

Funding

Medical Research Council MR/J010448/1
6 · The paper itself

Abstract

Mitochondria deserve special attention as sensors of cellular energy homeostasis and metabolic state. Moreover, mitochondria integrate intra- and extra-cellular signals to determine appropriate cellular responses that range from proliferation to cell death. In autoimmunity, as in other inflammatory chronic disorders, the metabolism of immune cells may be extensively remodeled, perturbing sensitive tolerogenic mechanisms. Here, we examine the distribution and effects of the therapeutic 21-mer peptide called P140, which shows remarkable efficacy in modulating immune responses in inflammatory settings. We measured P140 and control peptide effects on isolated mitochondria, the distribution of peptides in live cells, and their influence on the levels of key autophagy regulators. Our data indicate that while P140 targets macro- and chaperone-mediated autophagy processes, it has little effect, if any, on mitochondrial autophagy. Remarkably, however, it suppresses NET release from neutrophils exposed to immobilized NET-anti-DNA IgG complexes. Together, our results suggest that in the mitochondrion-lysosome axis, a likely driver of NETosis and inflammation, the P140 peptide does not operate by affecting mitochondria directly.

Indexed as

Adaptive ImmunityAnimalsAutophagyCells, CulturedExtracellular TrapsHumansImmunity, InnateIntravital MicroscopyLysosomesMiceMicroscopy, ConfocalMitochondriaMitophagyNeutrophilsPeptide FragmentsPrimary Cell CulturePeptide Fragmentsspliceosomal peptide P140autophagymitochondrionNETosisneuroinflammationP140 peptidesystemic lupus erythematosus

Identifiers

PMID30319621
PMCPMC6168670
OpenAlexW2893728150

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.