Evidence map›Paper›PMID 24022490›Full record

Trial reportThe Journal of biological chemistry2013

CR1-mediated ATP release by human red blood cells promotes CR1 clustering and modulates the immune transfer process.

Mark I Melhorn, Abigail S Brodsky, Jessica Estanislau, Joseph A Khoory, Ben Illigens, Itaru Hamachi, Yasutaka Kurishita, Andrew D Fraser, Anne Nicholson-Weller, Elena Dolmatova and 2 more

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Possible roles for ATP release from RBCs exclude the cAMP-mediated Panx1 pathway.American journal of physiology. Cell physiology · 2017
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. P2X and P2Y receptor signaling in red blood cells.Frontiers in molecular biosciences · 2015
    Review
  17. Article
  18. The pannexins: past and present.Frontiers in physiology · 2014
    Review
  19. Review
  20. Erythrocytes in multiple sclerosis - forgotten contributors to the pathophysiology?Multiple sclerosis journal - experimental, translational and clinical
    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 3 institutions in 2 countries.

Mark I MelhornFrom the Division of Allergy and Inflammation.
Abigail S Brodsky
Jessica Estanislau
Joseph A Khoory
Ben Illigens
Itaru Hamachi
Yasutaka Kurishita
Andrew D Fraser
Anne Nicholson-Weller
Elena Dolmatova
Heather S Duffy
Ionita C Ghiran
Kyoto University · JPBeth Israel Deaconess Medical Center · USOffice of Infectious Diseases · US

Funding

Modulation of erythrocyte function by complementR01HL096795 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI GHIRAN, IONITA CALIN · 2011 to 2014
$1.7M
NHLBI NIH HHS HL096795NHLBI NIH HHS R01 HL096795
6 · The paper itself

Abstract

Humans and other higher primates are unique among mammals in using complement receptor 1 (CR1, CD35) on red blood cells (RBC) to ligate complement-tagged inflammatory particles (immune complexes, apoptotic/necrotic debris, and microbes) in the circulation for quiet transport to the sinusoids of spleen and liver where resident macrophages remove the particles, but allow the RBC to return unharmed to the circulation. This process is called immune-adherence clearance. In this study we found using luminometric- and fluorescence-based methods that ligation of CR1 on human RBC promotes ATP release. Our data show that CR1-mediated ATP release does not depend on Ca(2+) or enzymes previously shown to mediate an increase in membrane deformability promoted by CR1 ligation. Furthermore, ATP release following CR1 ligation increases the mobility of the lipid fraction of RBC membranes, which in turn facilitates CR1 clustering, and thereby enhances the binding avidity of complement-opsonized particles to the RBC CR1. Finally, we have found that RBC-derived ATP has a stimulatory effect on phagocytosis of immune-adherent immune complexes.

Indexed as

Immunologic CappingAdenosine TriphosphateComplement System ProteinsErythrocytesFemaleHumansMaleMembrane LipidsPhagocytosisReceptors, Complement 3bAdenosine TriphosphateComplement System ProteinsCR1 protein, humanMembrane LipidsReceptors, Complement 3bATPCD47Immune AdherenceMK-571NeutrophilPannexin-1PhagocytosisProtein Kinase A (PKA)Protein Kinase C (PKC)Red Blood Cells

Identifiers

PMID24022490
PMCPMC3829426
OpenAlexW2014311252

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.