Evidence map›Paper›PMID 36030261›Full record

ArticleCell death & disease2022

Low quantity and quality of anti-spike humoral response is linked to CD4 T-cell apoptosis in COVID-19 patients.

Sonia André, Marne Azarias da Silva, Morgane Picard, Aurélie Alleaume-Buteau, Lucy Kundura, Renaud Cezar, Calaiselvy Soudaramourty, Santa Cruz André, Ana Mendes-Frias, Alexandre Carvalho and 17 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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
0.9field-weighted citation impact, top 25% 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, 9 citations in OpenAlex.

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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

27 authors at 7 institutions in 3 countries.

Sonia André *Université Paris Cité, INSERM U1124, F-75006, Paris, France.
Marne Azarias da Silva *Université Paris Cité, INSERM U1124, F-75006, Paris, France.
Morgane PicardUniversité Paris Cité, INSERM U1124, F-75006, Paris, France.
Aurélie Alleaume-ButeauUniversité Paris Cité, INSERM U1124, F-75006, Paris, France.
Lucy KunduraLaboratoire d'Immunologie, CHU de Nîmes, Nîmes, France.
Renaud CezarLaboratoire d'Immunologie, CHU de Nîmes, Nîmes, France.
Calaiselvy SoudaramourtyUniversité Paris Cité, INSERM U1124, F-75006, Paris, France.
Santa Cruz AndréLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.ORCID 0000-0002-5636-575X
Ana Mendes-FriasDepartment of Internal Medicine, Hospital of Braga, Braga, Portugal.
Alexandre CarvalhoLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.ORCID 0000-0001-5683-3181
Carlos CapelaLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.
Jorge PedrosaLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.
António Gil CastroLife and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.
Paul LoubetService des Maladies Infectieuses et Tropicales, CHU de Nîmes, Nîmes, France.
Albert SottoService des Maladies Infectieuses et Tropicales, CHU de Nîmes, Nîmes, France.
Laurent MullerService de Réanimation Chirugicale, CHU de Nîmes, Nîmes, France.
Jean-Yves LefrantService de Réanimation Chirugicale, CHU de Nîmes, Nîmes, France.ORCID 0000-0002-7774-2497
Claire RogerService de Réanimation Chirugicale, CHU de Nîmes, Nîmes, France.
Pierre-Géraud ClaretUrgences Médico-Chirugicales Hospitalisation, CHU de Nîmes, Nîmes, France.
Sandra DuvnjakService de Gérontologie et Prévention du Vieillissement, CHU de Nîmes, Nîmes, France.
Tu-Anh TranService de Pédiatrie, CHU de Nîmes, Nîmes, France.
Ouafa Zghidi-AbouzidCHU de Québec-Université Laval Research Center, Québec City, QC, Canada.
Pierre NiocheUniversité Paris Cité, INSERM U1124, F-75006, Paris, France.
Ricardo Silvestre *Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.
Pierre Corbeau *Laboratoire d'Immunologie, CHU de Nîmes, Nîmes, France. pierre.corbeau@igh.cnrs.fr.
Fabrizio Mammano *Université Paris Cité, INSERM U1124, F-75006, Paris, France. fabrizio.mammano@inserm.fr.ORCID 0000-0002-9193-7696
Jérôme Estaquier *Université Paris Cité, INSERM U1124, F-75006, Paris, France. estaquier@yahoo.fr.ORCID 0000-0002-9432-8044
Centre Hospitalier Universitaire de Nîmes · FRInserm · FRCentre National de la Recherche Scientifique · FRHospital Braga · PTUniversity of Minho · PTUniversité de Tours · FRUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to an inflammatory reaction, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)-infected patients present lymphopenia, which we recently reported as being related to abnormal programmed cell death. As an efficient humoral response requires CD4 T-cell help, we hypothesized that the propensity of CD4 T cells to die may impact the quantity and quality of the humoral response in acutely infected individuals. In addition to specific immunoglobulins (Ig)A, IgM, and IgG against SARS-CoV-2 nucleocapsid (N), membrane (M), and spike (S1) proteins, we assessed the quality of IgG response by measuring the avidity index. Because the S protein represents the main target for neutralization and antibody-dependent cellular cytotoxicity responses, we also analyzed anti-S-specific IgG using S-transfected cells (S-Flow). Our results demonstrated that most COVID-19 patients have a predominant IgA anti-N humoral response during the early phase of infection. This specific humoral response preceded the anti-S1 in time and magnitude. The avidity index of anti-S1 IgG was low in acutely infected individuals compared to convalescent patients. We showed that the percentage of apoptotic CD4 T cells is inversely correlated with the levels of specific IgG antibodies. These lower levels were also correlated positively with plasma levels of CXCL10, a marker of disease severity, and soluble Fas ligand that contributes to T-cell death. Finally, we found lower S-Flow responses in patients with higher CD4 T-cell apoptosis. Altogether, these results demonstrate that individuals with high levels of CD4 T-cell apoptosis and CXCL10 have a poor ability to build an efficient anti-S response. Consequently, preventing CD4 T-cell death might be a strategy for improving humoral response during the acute phase, thereby reducing COVID-19 pathogenicity.

Indexed as

Antibodies, ViralCD4-Positive T-LymphocytesCOVID-19Immunity, HumoralApoptosisHumansImmunoglobulin GSARS-CoV-2Spike Glycoprotein, CoronavirusAntibodies, ViralImmunoglobulin GSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2

Identifiers

PMID36030261
PMCPMC9419645
OpenAlexW4293325628

What OpenQuestion holds

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Registered trials

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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.