Цитокин-опосредованная дисрегуляция иммунного ответа при инфицировании SARS-CoV-2 (обзор)

Abstract

This review presents a hypothesis on the formation of cytokine-mediated dysregulation of immune response in humans upon introduction of coronavirus 2 (SARS-CoV-2) into the body. Some morphological features of this virus are highlighted, contributing to its penetration into the body and to the generation of a signal for the activation of antiviral immune defence. It has been determined that interleukins 1, 6 and 10 stimulate systemic inflammation, while interleukins 2, 7 and 15 regulate the adaptive immune responses of CD8+ T cells. The protective effect of interferons λ1–4 has been shown to alter the Th1/Th2 balance and thereby preserve immune homeostasis. However, in patients with COVID-19, CD8+ T cells demonstrate patterns of functional depletion amid an evolving cytokine storm. Nevertheless, with sufficient reserve capabilities of the immune system, an adaptive immune response can develop, potentiated by the body’s interferon, interleukin and humoral-cellular defence against SARS-CoV-2. However, against the background of cytokine-mediated dysregulation of T-cell immunity and progressive hyperinflammation in patients with a severe course of COVID-19, blood tests show pronounced leukopenia, acute-phase proteins, changes in the ratio between certain types of leukocytes, as well as a decrease in the number of T helper and T suppressor cells. The author believes such changes in human immune responses to be a result of an uncontrolled overproduction of cytokines that changed the body’s immune reactivity and resistance as well as caused a subsequently decreased synthesis of specific antibodies and a limited humoral response to the antigen. A conclusion is made that a timely elimination of the dysregulatory immune response is necessary to form an adequate humoral response and maintain high immunoreactivity in human populations, as well as to increase the body’s resistance and form a stable population immunity.