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<p>Complement overactivation, has been verified in COVID-19 patients. Complement regulatory proteins, including CD55, control complement overactivation thus eliminating complement deposition and cell lysis. We investigated complement regulatory protein expression in COVID-19 for potential deregulated expression patterns driving disease pathogenesis. Single-cell RNA-seq revealed increased PBMCs <i>CD55</i> expression in severely and critically ill patients. This increase was also detected upon integrated subclustering analysis of monocyte, T cell and B cell populations. FACS analysis confirmed the significant upregulation of CD55 expression in CD4<sup>+</sup> and CD8<sup>+</sup> T cells and monocyte populations of severely and critically ill COVID-19 patients. This upregulation was associated with decreased expression of type-I IFN-stimulated genes (ISGs) in patients with severe and critical COVID-19, indicating a suppressor effect of CD55. Silencing of <i>CD55</i> in T cells from COVID-19 severely ill patients in vitro and sensitization with SARS-CoV-2 peptides resulted in significantly augmented expression of ISGs and a reversal of their expression to levels similar to control or higher. The present study uncovers, to the best of our knowledge, a novel regulatory effect of CD55 on type-I IFN responses of severely ill COVID-19 patients, thus indicating its contribution to COVID-19 pathogenesis, and identifies a novel mechanistic pathway in the COVID-19 immune response.</p>

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CD55 upregulation in T cells of COVID-19 patients suppresses type-I interferon responses

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月2日

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  • Maria G. Detsika,
  • Maria Sakkou,
  • Vassiliki Triantafyllidou,
  • Dimitris Konstantopoulos,
  • Eirini Grigoriou,
  • Katherina Psarra,
  • Edison Jahaj,
  • Ioanna Dimopoulou,
  • Stylianos E. Orfanos,
  • Alexandra Tsirogianni,
  • George Kollias,
  • Anastasia Kotanidou

摘要

Complement overactivation, has been verified in COVID-19 patients. Complement regulatory proteins, including CD55, control complement overactivation thus eliminating complement deposition and cell lysis. We investigated complement regulatory protein expression in COVID-19 for potential deregulated expression patterns driving disease pathogenesis. Single-cell RNA-seq revealed increased PBMCs CD55 expression in severely and critically ill patients. This increase was also detected upon integrated subclustering analysis of monocyte, T cell and B cell populations. FACS analysis confirmed the significant upregulation of CD55 expression in CD4+ and CD8+ T cells and monocyte populations of severely and critically ill COVID-19 patients. This upregulation was associated with decreased expression of type-I IFN-stimulated genes (ISGs) in patients with severe and critical COVID-19, indicating a suppressor effect of CD55. Silencing of CD55 in T cells from COVID-19 severely ill patients in vitro and sensitization with SARS-CoV-2 peptides resulted in significantly augmented expression of ISGs and a reversal of their expression to levels similar to control or higher. The present study uncovers, to the best of our knowledge, a novel regulatory effect of CD55 on type-I IFN responses of severely ill COVID-19 patients, thus indicating its contribution to COVID-19 pathogenesis, and identifies a novel mechanistic pathway in the COVID-19 immune response.