| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T209 |
0-49 |
Sentence |
denotes |
T Cell Contribution to COVID-19 Hyperinflammation |
| T210 |
50-268 |
Sentence |
denotes |
While the induction of robust T cell immunity is likely essential for efficient virus control, dysregulated T cell responses may cause immunopathology and contribute to disease severity in COVID-19 patients (Figure 3). |
| T211 |
269-522 |
Sentence |
denotes |
This is suggested in a study by Zhou et al., which reported a significantly increased PBMC frequency of polyclonal GM-CSF+ CD4 T cells capable of prodigious ex vivo IL-6 and IFN-γ production only in critically ill COVID-19 patients (Zhou et al., 2020c). |
| T212 |
523-811 |
Sentence |
denotes |
Of note, GM-CSF+ CD4 T cells have been previously implicated in inflammatory autoimmune diseases, such as multiple sclerosis or juvenile rheumatoid arthritis, and high levels of circulating GM-CSF+ CD4 T cells were found to be associated with poor outcomes in sepsis (Huang et al., 2019). |
| T213 |
812-945 |
Sentence |
denotes |
Additionally, two studies observed reduced frequencies of Treg cells in severe COVID-19 cases (Chen et al., 2020c, Qin et al., 2020). |
| T214 |
946-1134 |
Sentence |
denotes |
Since Treg cells have been shown to help resolve ARDS inflammation in mouse models (Walter et al., 2018), a loss of Tregs might facilitate the development of COVID-19 lung immunopathology. |
| T215 |
1135-1392 |
Sentence |
denotes |
Similarly, a reduction of γδ-T cells, a subset of T cells with apparent protective antiviral function in influenza pneumonia (Dong et al., 2018, Zheng et al., 2013), has been reported in severely sick COVID-19 patients (Guo et al., 2020, Lei et al., 2020b). |
