| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T3 |
0-114 |
Sentence |
denotes |
The unique cytokine signature of COVID-19 might provide clues to disease mechanisms and possible future therapies. |
| T4 |
115-334 |
Sentence |
denotes |
Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild–moderate, severe–critical, and chronic–fibrotic). |
| T5 |
335-625 |
Sentence |
denotes |
In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. |
| T6 |
626-753 |
Sentence |
denotes |
Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. |
| T7 |
754-1000 |
Sentence |
denotes |
In severe COVID-19 cases, the IL-33–ST2 axis might act to expand the number of pathogenic granulocyte–macrophage colony-stimulating factor-expressing T cells, dampen antiviral interferon responses, elicit hyperinflammation, and favour thromboses. |
| T8 |
1001-1144 |
Sentence |
denotes |
In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. |
| T9 |
1145-1348 |
Sentence |
denotes |
We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target IL-33 (eg, anti-ST2), T helper 17-like γδ T cells, immune cell homing, and cytokine balance. |
