Evidence map›Paper›PMID 41573558›Full record

ArticleFrontiers in immunology2025

Contrasting immune responses in COVID-19: insights from healthcare workers and infected patients on plasmablast, pDC, and NK cell dynamics.

Laura Martín-Pedraza, Eulalia Rodríguez-Martín, Erick De La Torre-Tarazona, Elena Moreno, Roberto Pariente-Rodríguez, Paulette Esperanza Walo-Delgado, Javier García-Pérez, Jorge Díaz, Laura Luna, Mario Rodríguez-Dominguez and 9 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

19 authors.

Laura Martín-PedrazaServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Eulalia Rodríguez-MartínServicio de Inmunología, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain.
Erick De La Torre-TarazonaServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Elena MorenoServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Roberto Pariente-RodríguezServicio de Inmunología, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain.
Paulette Esperanza Walo-DelgadoServicio de Inmunología, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain.
Javier García-PérezLaboratorio de Referencia e Investigación en Retrovirus, Instituto de Salud Carlos III, CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Jorge DíazServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Laura LunaServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Mario Rodríguez-DominguezServicio de Microbiología, Hospital Ramón y Cajal, IRYCIS, y CIBER en Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.
Juan Carlos GalánServicio de Microbiología, Hospital Ramón y Cajal, IRYCIS, y CIBER en Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.
Claudia Geraldine RitaServicio de Inmunología, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain.
Ana Del Amo-de PalaciosServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Roser Navarro-SolerServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
María FonsServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
José AlcamíLaboratorio de Referencia e Investigación en Retrovirus, Instituto de Salud Carlos III, CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Santiago MorenoServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.
Luisa María VillarServicio de Inmunología, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain.
Sergio Serrano-VillarServicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, IRYCIS, Universidad de Alcalá y CIBER de Enfermedades Infecciosas (CIBERINFEC), Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The COVID-19 pandemic, caused by SARS-CoV-2, has highlighted significant variability in disease severity, ranging from asymptomatic cases to severe acute respiratory distress syndrome. Objective: Understanding the immune responses that contribute to this variability, particularly among healthcare workers (HCWs) frequently exposed to the virus, is essential. Materials and methods: This was a prospective single-center longitudinal cohort study. We included hospitalized COVID-19+ patients, classified as having mild or moderate-to-severe symptoms, and unvaccinated HCWs with low susceptibility. Peripheral blood mononuclear cells (PBMCs) were collected and analyzed using flow cytometry. We measured the frequencies of key immune subsets, including plasmablasts, plasmacytoid dendritic cells (pDCs), and Natural Killer (NK) cells. SARS-CoV-2 neutralizing antibodies (NAbs) were quantified using pseudotyped HIV particles. Results: COVID-19+ patients exhibited a significant increase in plasmablasts, a B-cell subset responsible for producing neutralizing antibodies, which correlated with disease severity (p=0.0082). Conversely, uninfected HCWs had low levels of plasmablasts but significantly higher levels of plasmacytoid dendritic cells (pDCs) (p<0.0001), which produce interferons upon activation by viral antigens. Additionally, HCWs had a higher percentage of CD56bright NK cells than the susceptible patients (p=0.02). Conclusion: Our findings suggest that immune dysregulation, characterized by increased plasmablasts and reduced pDC and NK cell responses, contributes to COVID-19 severity. Strong pDC and NK cell responses may confer protection against SARS-CoV-2. These insights into immune responses may inform strategies for therapeutic interventions and vaccine development.

Indexed as

COVID-19Dendritic CellsHealth PersonnelKiller Cells, NaturalPlasma CellsSARS-CoV-2AdultAntibodies, NeutralizingAntibodies, ViralFemaleHumansLongitudinal StudiesMaleMiddle AgedProspective StudiesAntibodies, NeutralizingAntibodies, ViralCOVID-19dendritic cellshealthcare workersimmune responseNK cellsplasmablastsSARS-CoV-2

Identifiers

PMID41573558
PMCPMC12819764

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.