| T16 |
54-1130 |
Sentence |
denotes |
Whereas virus-induced MAS shows the classic hallmarks of a T-helper (Th)-1 profile, with high production of IFNγ,1, 3 COVID-19 is instead characterised by circulating T cells that show an activated Th17 membrane phenotype (CD38+HLA-DR+CD4+CCR6+)4 and express granulocyte–macrophage colony-stimulating factor (GM-CSF) in part along with IFNγ.5 Concentrations of both IL-17 and IFNγ are increased in serum from patients with COVID-19 in proportion with viral load and lung injury.6 Similarly, Middle East respiratory syndrome has been associated with a combined Th1–Th17 inflammatory response.7 Notably, the cytokine storm composition induced by SARS-CoV-2 differs from that induced by severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus, with lower production of type 1 cytokines (eg, IL-12p70, IL-15), and high concentrations of type 2 cytokines (eg, IL-4, IL-9, IL-10, transforming growth factor β [TGFβ], IL-13).6, 7, 8, 9, 10, 11 These findings might provide important clues to the specific immunopathology of COVID-19. |
| T18 |
1373-2201 |
Sentence |
denotes |
In the lungs, IL-33 is promptly released, mainly by injured epithelial alveolar cells, following infection and cellular damage.12 Among its functions, IL-33 enhances TGFβ-mediated differentiation of Foxp3+ regulatory T (Treg) cells13 and stimulates CD11c+ myeloid dendritic cells to secrete IL-2, which drives Treg cell expansion, thus ultimately promoting resolution of inflammation.14 Individuals infected with SARS-CoV-2 who develop milder symptoms tend to have large numbers of Treg cells10 and alveolar macrophages showing a scavenger resolving (FABP4+) phenotype.15 In the presence of an adequate immune response and virus clearance, IL-33 might drive rapid Treg cell-dependent restoration of respiratory tissue homoeostasis, which probably accounts for the mild or asymptomatic forms of COVID-19 seen in most individuals. |
