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Current review presents a brief overview of the immune system dysregulation during acute COVID-19 and illustrates the main alterations in peripheral blood CD4+ T-cell (Th) subsets and their target cells. Dendritic cell dysfunction effects induced by SARS-CoV-2 exhibited decreased expression of cell-surface HLA-DR, CCR7 and co-stimulatory molecules CD80 and CD86, indicating a reduction of antigen presenting, migrating and activation capacities of peripheral blood dendritic cells. SARS-CoV-2-specific Th cells could be detected as early as days 2–4 post-symptom onset, while the extended absence of SARS-CoV-2-specific Th cells was associated with severe and/or poor COVID-19 outcome. Firstly, in acute COVID-19 the frequency of Th1 cell was comparable with control levels, but several studies have reported an upregulation of inhibitory immune checkpoint receptors and exhaustion-associated molecules (TIM3, PD-1, BTLA, TIGIT etc.) on circulating CD8+ T-cells and NK-cell, while the level of macrophage was increased in bronchoalveolar lavage (BAL) samples. Next, type 2 immune responses are mediated mainly by Th2 cells, and several studies have revealed a skewing towards Th2 in peripheral blood samples from patients with acute COVID-19. Furthermore, the decreases of circulating main Th2 target cells – basophiles and eosinophils – were associated with severe COVID-19, while the lung tissue was enriched with mast cells and their mediators, that were realized during degranulation. Moreover, the frequencies of peripheral blood Th17 cell were closely linked with COVID-19 severity, thus, low levels of Th17 cell were observed in patients with severe COVID-19, but in BAL the relative numbers of Th17 cell as well as the concentrations of their effector cytokines were dramatically increased. It was shown that severe COVID-19 patients had higher relative numbers of neutrophils if compared with healthy controls, and the majority of patients with COVID-19 had increased frequencies and absolute numbers of immature neutrophils with altered ROS production. Finally, the frequencies of Tfh cells was decreased during acute COVID-19 infection. Elevated numbers of activated Tfh were found as well as the alterations in Tfh cell subsets characterized by the decrease of ‘regulatory’ Tfh1 cell and increase of ‘pro-inflammatory’ Tfh2 and Tfh17 cell subsets were revealed. Descriptions of peripheral blood B cells during an acute SARS-CoV-2 infection had reported the relative B cell lymphopenia with the decreased frequencies of ‘naïve’ and memory B cell subsets, as well as increased levels of CD27hiCD38hiCD24− plasma cell precursors and atypical CD21low B cells. Thus, the emerging evidences indicate that functional alterations occur in all Th cell subsets, and they are linked with loss-of-functions of main Th cell subsets target cells. Furthermore, recovered individuals could suffer from long-term immune responses dysregulation and other persistent symptoms for many months even after SARS-CoV-2 elimination, a condition referred to as post-acute COVID-19 syndrome.

About the authors

I. Kudryavtsev

Pavlov First St. Petersburg State Medical University, St.Petersburg, Russian Federation; Institute of Experimental Medicine (FSBSI "IEM"), St.Petersburg, Russian Federation

Author for correspondence.
Email: igorek1981@yandex.ru

PhD (Biology), assistant professor of department of Immunology, Pavlov First St. Petersburg State Medical University, St.Petersburg, Russian Federation; head of laboratory, Institute of Experimental Medicine (FSBSI "IEM"), St.Petersburg, Russian Federation

Russian Federation

A. Golovkin

V.A. Almazov National Medical Research Centre, St.Petersburg, Russian Federation

Email: golovkin_a@mail.ru

PhD, MD (Medicine), Head of a Research Group, Institute of Molecular Biology and Genetics

Russian Federation

A. Totolian

Pavlov First St. Petersburg State Medical University, St.Petersburg, Russian Federation; St. Petersburg Pasteur Institute, St. Petersburg, Russian Federation.

Email: totolian@pasteurorg.ru

RAS Full Member, PhD, MD (Medicine), Professor, Head of the department of immunology, Pavlov First St. Petersburg State Medical University; Director of St. Petersburg Pasteur Institute.

Russian Federation


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