Marked T cell activation, senescence, exhaustion and skewing towards TH17 in patients with COVID-19 pneumonia

By S. De Biasi, M. Meschiari, L. Gibellini, Caterina Bellinazzi, R. Borella, L. Fidanza, L. Gozzi, A. Iannone, D. Lo Tartaro, M. Mattioli and 18 more. Nature Communications, 2020

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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+CD57+ 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+ 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. COVID-19 is a serious pandemic threat to public health, but insights on the pathophysiological and immunological conditions are only emerging. Here the authors use multi-color flow cytometry to characterize CD4+ and CD8+ T cells in peripheral blood from 39 COVID-19 patients in Italy to report altered T cell activation, function and polarization.

Subfields: Infectious Diseases, Neurology

View Paper: https://www.semanticscholar.org/paper/a07900d9715fe3781cd50b0f6b12cde1fa4bbe28

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