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Background <p>Dysregulation of the innate immune response to SARS-CoV-2 has been linked to poor outcomes in COVID-19. Neutrophils are key players in this response, displaying distinct functional profiles associated with disease severity. This study investigates how neutrophil phenotypes, and their mediators are modulated in severe COVID-19 following vaccination.</p> Methods and Results <p>We conducted an observational case-control study using clinical data, serum samples, and circulating neutrophils from patients hospitalized with severe COVID-19. Neutrophils from vaccinated patients exhibited increased expression of surface markers including TREM-1, CD182, HLA-DR, and PD-L1, alongside higher HLA-DR mean fluorescence intensity (MFI). These cells also showed a higher proportion of inflammatory (CD16⁺CD182⁺TREM-1⁺) and immunoregulatory (HLA-DR⁺PD-L1⁺) subsets compared to non-vaccinated individuals. Exploratory principal component analysis (PCA) revealed a trend toward separation of vaccinated and non-vaccinated groups, suggestively driven by inflammatory cytokines (IL-6, TNF-α, GM-CSF, IL-18) and neutrophil surface markers (HLA-DR, PD-L1, TREM-1, CD16).</p> Conclusions <p>These findings suggest that prior COVID-19 vaccination is associated with a distinct neutrophil activation profile in patients with severe disease, characterized by the concomitant expression of pro-inflammatory and immunoregulatory markers. This immune phenotype may reflect a more balanced inflammatory response during severe SARS-CoV-2 infection. These findings open avenues for future studies incorporating functional assays and larger, independent cohorts to confirm and extend the biological and clinical relevance of these observations.</p>

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COVID-19 vaccination shifts neutrophils toward a mixed activated and regulatory phenotype in patients with severe disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月11日

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  • Yrna Lorena M. de Oliveira,
  • Ayane de S. Resende,
  • Mariana N. F. de Franca,
  • Camilla Natália O. Santos,
  • Lucas S. Magalhães,
  • Cristiane B. Correa,
  • Priscila L. dos S. Almeida,
  • Angela Maria da Silva,
  • Michael W. Lipscomb,
  • Tatiana R. de Moura

摘要

Background

Dysregulation of the innate immune response to SARS-CoV-2 has been linked to poor outcomes in COVID-19. Neutrophils are key players in this response, displaying distinct functional profiles associated with disease severity. This study investigates how neutrophil phenotypes, and their mediators are modulated in severe COVID-19 following vaccination.

Methods and Results

We conducted an observational case-control study using clinical data, serum samples, and circulating neutrophils from patients hospitalized with severe COVID-19. Neutrophils from vaccinated patients exhibited increased expression of surface markers including TREM-1, CD182, HLA-DR, and PD-L1, alongside higher HLA-DR mean fluorescence intensity (MFI). These cells also showed a higher proportion of inflammatory (CD16⁺CD182⁺TREM-1⁺) and immunoregulatory (HLA-DR⁺PD-L1⁺) subsets compared to non-vaccinated individuals. Exploratory principal component analysis (PCA) revealed a trend toward separation of vaccinated and non-vaccinated groups, suggestively driven by inflammatory cytokines (IL-6, TNF-α, GM-CSF, IL-18) and neutrophil surface markers (HLA-DR, PD-L1, TREM-1, CD16).

Conclusions

These findings suggest that prior COVID-19 vaccination is associated with a distinct neutrophil activation profile in patients with severe disease, characterized by the concomitant expression of pro-inflammatory and immunoregulatory markers. This immune phenotype may reflect a more balanced inflammatory response during severe SARS-CoV-2 infection. These findings open avenues for future studies incorporating functional assays and larger, independent cohorts to confirm and extend the biological and clinical relevance of these observations.