tetano
Editor, Senior Moderator
Commun Biol
. 2025 May 2;8(1):690.
doi: 10.1038/s42003-025-08066-z. CD55 upregulation in T cells of COVID-19 patients suppresses type-I interferon responses
Maria G Detsika[SUP] 1 [/SUP], Maria Sakkou[SUP] 2 3 4 [/SUP], Vassiliki Triantafyllidou[SUP] 2 [/SUP], Dimitris Konstantopoulos[SUP] 2 [/SUP], Eirini Grigoriou[SUP] 5 [/SUP], Katherina Psarra[SUP] 5 [/SUP], Edison Jahaj[SUP] 6 [/SUP], Ioanna Dimopoulou[SUP] 6 [/SUP], Stylianos E Orfanos[SUP] 6 [/SUP], Alexandra Tsirogianni[SUP] 5 [/SUP], George Kollias[SUP] 2 3 4 [/SUP], Anastasia Kotanidou[SUP] 7 [/SUP]
Affiliations
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[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 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.
. 2025 May 2;8(1):690.
doi: 10.1038/s42003-025-08066-z. CD55 upregulation in T cells of COVID-19 patients suppresses type-I interferon responses
Maria G Detsika[SUP] 1 [/SUP], Maria Sakkou[SUP] 2 3 4 [/SUP], Vassiliki Triantafyllidou[SUP] 2 [/SUP], Dimitris Konstantopoulos[SUP] 2 [/SUP], Eirini Grigoriou[SUP] 5 [/SUP], Katherina Psarra[SUP] 5 [/SUP], Edison Jahaj[SUP] 6 [/SUP], Ioanna Dimopoulou[SUP] 6 [/SUP], Stylianos E Orfanos[SUP] 6 [/SUP], Alexandra Tsirogianni[SUP] 5 [/SUP], George Kollias[SUP] 2 3 4 [/SUP], Anastasia Kotanidou[SUP] 7 [/SUP]
Affiliations
- PMID: 40316776
- PMCID: PMC12048498
- DOI: 10.1038/s42003-025-08066-z
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[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 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.