| T59 |
0-1168 |
Sentence |
denotes |
Although described as Th1 cells, at least half of the GM-CSF-producing T cells observed in the circulation of patients with severe COVID-19 do not coexpress the canonical Th1 cytokine IFNγ.5 Lymphocytes from patients with COVID-19 appear to be functionally exhausted, producing lower amounts of IFNγ, IL-2, and tumour necrosis factor (TNF), and having decreased cytotoxic function.29 Many factors could possibly explain this lymphocyte dysfunction, in particular the upregulation of multiple coinhibitory receptors such as CD94, CD152 (cytotoxic T-lymphocyte-associated antigen 4), programmed cell death protein 1 (PD-1), and T-cell immunoglobulin mucin receptor 3 (TIM-3).29 However, suboptimal production of IFNγ, poor cytotoxic capabilities, a shorter lymphocyte lifespan, and lymphopenia might also be attributable to a scarcity in type I and III interferons (IFNα, IFNβ, and IFNλ), in the blood as well as in the lungs of patients with COVID-19.27 Interferons are more highly suppressed by SARS-CoV-2 than by SARS-CoV infection,27, 28 and this most likely accounts for the impaired antiviral responses and spontaneous apoptosis of dysfunctional lymphocytes.11, 30 |
