Immune phenotypes that predict COVID-19 severity.
Thomas LiechtiYaser IftikharMassimo ManginoMargaret BeddallCharles GossJane A O'HalloranPhilip A MuddMario RoedererPublished in: Research square (2022)
Severe COVID-19 causes profound immune perturbations, but pre-infection immune signatures contributing to severe COVID-19 remain unknown. Genome-wide association studies (GWAS) identified strong associations between severe disease and several chemokine receptors and molecules from the type I interferon pathway. Here, we define immune signatures associated with severe COVID-19 using high-dimensional flow cytometry. We measured the peripheral immune system from individuals who recovered from mild, moderate, severe or critical COVID-19 and focused only on those immune signatures returning to steady-state. Individuals that suffered from severe COVID-19 showed reduced frequencies of T cell, MAIT cell and dendritic cell (DCs) subsets and altered chemokine receptor expression on several subsets, such as reduced levels of CCR1 and CCR2 on monocyte subsets. Furthermore, we found reduced frequencies of type I interferon-producing plasmacytoid DCs and altered IFNAR2 expression on several myeloid cells in individuals recovered from severe COVID-19. Thus, these data identify potential immune mechanisms contributing to severe COVID-19.
Keyphrases
- coronavirus disease
- dendritic cells
- sars cov
- early onset
- regulatory t cells
- respiratory syndrome coronavirus
- immune response
- flow cytometry
- peripheral blood
- stem cells
- induced apoptosis
- machine learning
- endothelial cells
- mesenchymal stem cells
- poor prognosis
- gene expression
- electronic health record
- cell death
- acute myeloid leukemia
- dna methylation
- climate change
- artificial intelligence
- cell cycle arrest