Marked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumonia
説明
<jats:title>Abstract</jats:title><jats:p>The immune system of patients infected by SARS-CoV-2 is severely impaired. Detailed investigation of T cells and cytokine production in patients affected by COVID-19 pneumonia are urgently required. Here we show that, compared with healthy controls, COVID-19 patients’ T cell compartment displays several alterations involving naïve, central memory, effector memory and terminally differentiated cells, as well as regulatory T cells and PD1<jats:sup>+</jats:sup>CD57<jats:sup>+</jats:sup> exhausted T cells. Significant alterations exist also in several lineage-specifying transcription factors and chemokine receptors. Terminally differentiated T cells from patients proliferate less than those from healthy controls, whereas their mitochondria functionality is similar in CD4<jats:sup>+</jats:sup> T cells from both groups. Patients display significant increases of proinflammatory or anti-inflammatory cytokines, including T helper type-1 and type-2 cytokines, chemokines and galectins; their lymphocytes produce more tumor necrosis factor (TNF), interferon-γ, interleukin (IL)-2 and IL-17, with the last observation implying that blocking IL-17 could provide a novel therapeutic strategy for COVID-19.</jats:p>
収録刊行物
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- Nature Communications
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Nature Communications 11 (1), 3434-, 2020-07-06
Springer Science and Business Media LLC
