TABLE 2.

Key evidence for transforming growth factor-beta (TGF-β) as a mediator of COVID-19 immune dysregulation and thrombosis.

References	Key findings
Park et al. (79)	TGFβIp acetylated at Lysine 676 is a diagnostic marker of severity in SARS-CoV-2 pneumonia
Sacchi et al. (83)	Polymorphonuclear myeloid-derived suppressor cells inhibit T-cell IFN-λ production during SARS-CoV-2 peptide stimulation through TGFβ mechanisms
Ghazavi et al. (82)	Serum TGFβ levels increase with increasing disease severity in patients with COVID-19
Kvedaraite et al. (99)	Serum TGFβ levels correlate with circulating monocyte phenotype in severe COVID-19
Ferreira-Gomes et al. (80)	SARS-CoV-2 triggers an immune response instructed by TGFβ, including IgA class switching
D’Agnillo et al. (95)	TGFβ1 staining co-localizes with PAI-1 in pulmonary blood vessels and developing fibrotic lesions in COVID-19 lung tissue
Witkowski et al. (78)	Serum levels of TGFβ peak during the first 2 weeks of severe COVID-19 infection and inhibit NK cell function
Colarusso et al. (97)	Higher TGFβ levels predict an increased relative risk of lung fibrosis-like changes in post-COVID patients
Vaz de Paula et al. (96)	Immuno-expression of TGFβ1 is increased in lung tissue of patients who died of COVID-19
Dinnon et al. (109)	Transcriptomic analysis of diseased alveolar regions shows up-regulated signaling by the TGFβ receptor complex in mouse-adapted SARS-CoV-2
Colarusso et al. (98)	TGFβ has higher stimulated release in post-COVID patients with signs of lung fibrosis on chest computed tomography scans

All listed studies are cited in the references section. TGF-β, transforming growth factor beta; LLC, large latent complex; NK, natural killer; PAI-I, plasminogen activator inhibitor; TGFβIp, TGFβ induced protein.