Regulatory T cells: A potential weapon to combat COVID-19?

Abstract

Since the end of December 2019, a novel coronavirus SARS-CoV-2 began to spread, an infection disease termed COVID-19. The virus has spread throughout the world in a short period of time, resulting in a pandemic. The number of reported cases in global reached 5 695 596 including 352 460 deaths, as of May 27, 2020. Due to the lack of effective treatment options for COVID-19, various strategies are being tested. Recently, pathologic studies conducted by two teams in China revealed immunopathologic abnormalities in lung tissue. These results have implications for immunotherapy that could offer a novel therapy strategy for combating lethal viral pneumonia. This review discusses the clinical and pathological features of COVID-19, the roles of immune cells in pathological processes, and the possible avenues for induction of immunosuppressive T regulatory cells attenuating lung inflammation due to viral infection. It is our hope that these proposals may both be helpful in understanding the novel features of SARS-CoV-2 pneumonia as well as providing new immunological strategies for treating the severe sequelae of disease manifestations seen in people infected with SARS-CoV-2.

Keywords: 2019 novel coronavirus; SRAS‐CoV‐2; Tregs; pathology; pneumonia.

FIGURE 1

Immune response in lung tissues after coronavirus infection. When lung tissue is infected with coronavirus, NK cells, macrophages, and antigen‐presenting cells are recruited to the tissue to produce inflammatory factors and then active CD8 and CD4 T cells for combat coronavirus. When the infection is serious, these inflammatory factors will form inflammatory cytokines storm to injury the tissue. TNF‐α, IL‐1β, IL‐6, and IL‐8 are considered the main components of cytokine‐storm. TNF‐α would be produced by NK cells, macrophages, and activated CD4 and CD8 T cells. IL‐1β and IL‐8 are secreted by macrophages. IL‐6 could be produced by inflammatory macrophages. At the same time, T cells also secrete IFN‐γ to fight the coronavirus. On the opposite side, Treg and type II macrophage could secret IL‐10 and TGF‐β, which then reduce inflammatory response. In addition, TGF‐β participates in the tissue repair process