Evidence map›Paper›PMID 41190065›Full record

ArticleFrontiers in immunology2025

CD39 is an antibody-secreting B-cell marker that modulates germinal center and antibody responses during infection.

Laura Almada, Yamila N Gazzoni, Cristian G Beccaria, Facundo Fiocca Vernengo, Santiago Boccardo, Melisa Gorosito Serrán, Apurwa Trivedi, Carola G Vinuesa, Simon C Robson, Eva V Acosta Rodríguez and 3 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Laura AlmadaDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Yamila N GazzoniDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Cristian G BeccariaDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Facundo Fiocca VernengoDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Santiago BoccardoDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Melisa Gorosito SerránDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Apurwa TrivediCentre d'Immunologie de Marseille-Luminy (CIML), Aix Marseille Université, Institut national de la santé et de la recherche médicale (INSERM), Centre national de la recherche scientifique (CNRS),, Marseille, France.
Carola G VinuesaJohn Curtin School of Medical Research (JCSMR), Canberra, ACT, Australia.
Simon C RobsonCenter for Inflammation Research, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Eva V Acosta RodríguezDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Mauro GayaCentre d'Immunologie de Marseille-Luminy (CIML), Aix Marseille Université, Institut national de la santé et de la recherche médicale (INSERM), Centre national de la recherche scientifique (CNRS),, Marseille, France.
Carolina L MontesDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.
Adriana GruppiDepartamento de Bioquímica Clínica, Facultad de Ciencias Químicas (FCQ), Universidad Nacional de Córdoba, Córdoba, Argentina.

Funding

Antibody-secreting cells in the regulation of T cell response to Trypanosoma cruziR01AI116432 · NIAID · NATIONAL RESEARCH COUNCIL OF ARGENTINA · PI ADRIANA GRUPPI · 2015 to 2026
$1.3M
NIAID NIH HHS R01 AI116432
6 · The paper itself

Abstract

CD39 is an ectoenzyme in immune cells that regulates purinergic signaling by converting extracellular ATP into adenosine (ADO). Although first described on EBV-transformed B cells, CD39's role in humoral immunity remains unclear. Using murine infection models and human samples, we confirm and extend previous findings showing that high CD39 expression identifies antibody-secreting cells (ASC) across differentiation stages, including ASC derived from memory B cells, and in various tissues, regardless of the infection phase. CD39 was resistant to enzymatic digestion, facilitating ASC identification in processed tissues. We found that while CD39 was not essential for B-cell differentiation into ASC, it remained functionally active as an ectoenzyme. ASC as well as germinal center (GC) B cells expressed ADO receptors, making them responsive to ADO signaling. Consistently, systemic ADO administration impaired GC reactions without altering the ASC number in infected mice. However,

Indexed as

Antibody FormationAntibody-Producing CellsAntigens, CDApyraseB-LymphocytesGerminal CenterAdenosineAnimalsBiomarkersCell DifferentiationHumansImmunity, HumoralLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutAdenosineAntigens, CDApyraseBiomarkersCD39 antigenADOantibody secreting cell (ASC)germinal center (GC)influenza virusplasmablastplasma cell (PC)Trypanosoma cruzi

Identifiers

PMID41190065
PMCPMC12580622

What Socratic 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 Socratic graph.