Evidence map›Paper›PMID 32886698›Full record

ArticlePloS one2020

Memory CD73+IgM+ B cells protect against Plasmodium yoelii infection and express Granzyme B.

Marcela Parra, Megan Weitner, Amy Yang, Adovi Akue, Xia Liu, Thomas Schmidt, Windy R Allman, Mustafa Akkoyunlu, Steven C Derrick

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. IgMJournal of leukocyte biology · 2022
    Article
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

9 authors at 1 institution in 1 country.

Marcela ParraUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Megan WeitnerUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Amy YangUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Adovi AkueUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Xia LiuUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Thomas SchmidtUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Windy R AllmanUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Mustafa AkkoyunluUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.
Steven C DerrickUnited States Food and Drug Administration, Center for Biologics and Research, Division of Bacterial, Parasitic and Allergenic Diseases, Silver Spring, Maryland, United States of America.ORCID 0000-0001-8112-8644
Center for Biologics Evaluation and Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To better understand anti-malaria protective immune responses, we examined the cellular mechanisms that govern protective immunity in a murine Plasmodium yoelii 17X NL (PyNL) re-infection model. Initially, we confirmed that immune B cells generated during a primary PyNL infection were largely responsible for protection from a second PyNL infection. Using the previously identified memory B cell markers CD80, PD-L2, and CD73, we found an increase in the frequency of CD80-PD-L2-CD73+ B cells up to 55 days after a primary PyNL infection and at 4-6 days following a second PyNL infection. Moreover, injection of enriched immune CD19+CD73+ B cells into nonimmune mice were significantly more protective against a PyNL infection than CD73- B cells. Interestingly, a substantial fraction of these CD73+ B cells also expressed IgM and granzyme B, a biomolecule that has been increasingly associated with protective responses against malaria.

Indexed as

5'-NucleotidaseAnimalsAntigens, CD19B-LymphocytesFemaleGranzymesImmunityImmunoglobulin MMalariaMiceMice, Inbred BALB CPlasmodium yoelii5'-NucleotidaseAntigens, CD19CD19 antigen, mouseGranzymesGZMB protein, humanImmunoglobulin M

Identifiers

PMID32886698
PMCPMC7473529
OpenAlexW3083334133

What OpenQuestion holds

Textmetadata
LicenceCC0
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.