Evidence map›Paper›PMID 37316832›Full record

ArticleBMC medicine2023

Efficacy of COVID-19 mRNA vaccination in patients with autoimmune disorders: humoral and cellular immune response.

Federica Filippini, Mauro Giacomelli, Chiara Bazzani, Micaela Fredi, Paolo Semeraro, Cesare Tomasi, Franco Franceschini, Arnaldo Caruso, Ilaria Cavazzana, Cinzia Giagulli

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Vaccination Update and Specific Concerns for RA.Current rheumatology reports · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. 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

10 authors at 2 institutions in 1 country.

Federica FilippiniSection of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0003-1598-8317
Mauro GiacomelliSection of Microbiology, ASST Spedali Civili of Brescia, 25123, Brescia, Italy.
Chiara BazzaniRheumatology and Clinical Immunology, ASST Spedali Civili of Brescia, Brescia, Italy.ORCID 0000-0002-7710-6693
Micaela FrediRheumatology and Clinical Immunology, ASST Spedali Civili of Brescia and Department of Clinical and Experimental Sciences, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0002-6511-4936
Paolo SemeraroRheumatology and Clinical Immunology, ASST Spedali Civili of Brescia and Department of Clinical and Experimental Sciences, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0002-7053-3086
Cesare TomasiRheumatology and Clinical Immunology, ASST Spedali Civili of Brescia and Department of Clinical and Experimental Sciences, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0002-3699-8744
Franco FranceschiniRheumatology and Clinical Immunology, ASST Spedali Civili of Brescia and Department of Clinical and Experimental Sciences, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0003-3678-6124
Arnaldo CarusoSection of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0001-5178-566X
Ilaria Cavazzana *Rheumatology and Clinical Immunology, ASST Spedali Civili of Brescia, Brescia, Italy. ilaria.cavazzana@unibs.it.ORCID 0000-0002-2757-7120
Cinzia Giagulli *Section of Microbiology, Department of Molecular and Translational Medicine, University of Brescia, 25123, Brescia, Italy.ORCID 0000-0002-4461-9353
University of Brescia · ITAzienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe impact of immunosuppressive therapies on the efficacy of vaccines to SARS-CoV-2 is not completely clarified. We analyzed humoral and T cell-mediated response after COVID-19 mRNA vaccine in immunosuppressed patients and patients with common variable immunodeficiency disease (CVID). PATIENTS: We enrolled 38 patients and 11 healthy sex- and age-matched controls (HC). Four patients were affected by CVID and 34 by chronic rheumatic diseases (RDs). All patients with RDs were treated by corticosteroid therapy and/or immunosuppressive treatment and/or biological drugs: 14 patients were treated with abatacept, 10 with rituximab, and 10 with tocilizumab.

methodsTotal antibody titer to SARS-CoV-2 spike protein was assessed by electrochemiluminescence immunoassay, CD4 and CD4-CD8 T cell-mediated immune response was analyzed by interferon-γ (IFN-γ) release assay, the production of IFN-γ-inducible (CXCL9 and CXCL10) and innate-immunity chemokines (MCP-1, CXCL8, and CCL5) by cytometric bead array after stimulation with different spike peptides. The expression of CD40L, CD137, IL-2, IFN-γ, and IL-17 on CD4 and CD8 T cells, evaluating their activation status, after SARS-CoV-2 spike peptides stimulation, was analyzed by intracellular flow cytometry staining. Cluster analysis identified cluster 1, namely the "high immunosuppression" cluster, and cluster 2, namely the "low immunosuppression" cluster.

resultsAfter the second dose of vaccine, only abatacept-treated patients, compared to HC, showed a reduced anti-spike antibody response (mean: 432 IU/ml ± 562 vs mean: 1479 IU/ml ± 1051: p = 0.0034), and an impaired T cell response, compared with HC. In particular, we found a significantly reduced release of IFN-γ from CD4 and CD4-CD8 stimulated T cells, compared with HC (p = 0.0016 and p = 0.0078, respectively), reduced production of CXCL10 and CXCL9 from stimulated CD4 (p = 0.0048 and p = 0.001) and CD4-CD8 T cells (p = 0.0079 and p = 0.0006). Multivariable General Linear Model analysis confirmed a relationship between abatacept exposure and impaired production of CXCL9, CXCL10, and IFN-γ from stimulated T cells. Cluster analysis confirms that cluster 1 (including abatacept and half of rituximab treated cases) showed a reduced IFN-γ response, as well as reduced monocyte-derived chemokines All groups of patients demonstrated the ability to generate specific CD4 T activated cells after spike proteins stimulation. After the third dose of vaccine, abatacept-treated patients acquired the ability to produce a strong antibody response, showing an anti-S titer significantly higher compared to that obtained after the second dose (p = 0.0047), and comparable with the anti-S titer of the other groups.

conclusionsPatients treated with abatacept showed an impaired humoral immune response to two doses of COVID-19 vaccine. The third vaccine dose has been demonstrated to be useful to induce a more robust antibody response to balance an impaired T cell-mediated one. All patients, exposed to different immunosuppressive drugs, were able to produce specific CD4-activated T cells, after spike proteins stimulation.

trial registrationLocal Ethical Committee NP4187.

Indexed as

Autoimmune DiseasesCOVID-19AbataceptCOVID-19 VaccinesHumansImmunity, CellularImmunosuppressive AgentsRituximabRNA, MessengerSARS-CoV-2Spike Glycoprotein, CoronavirusVaccinationAbataceptCOVID-19 VaccinesImmunosuppressive AgentsRituximabRNA, MessengerSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2AbataceptAutoimmune diseasesCOVID-19 vaccinationInterferon-γRituximabT cell

Identifiers

PMID37316832
PMCPMC10266318
OpenAlexW4380628233

What OpenQuestion holds

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LicenceCC BY
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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.