Peripheral innate and adaptive immune cells during COVID-19: Functional neutrophils, pro-inflammatory monocytes and half-dead lymphocytes

Abstract

A better understanding of the innate and adaptive cells in the COVID-19 disease caused by the SARS-CoV-2 coronavirus is a necessity for the development of effective treatment methods and vaccines. We studied phenotypic features of innate and adaptive immune cells, oxidative burst, phagocytosis and apoptosis. One hundred and three patients with COVID-19 grouped according to their clinical features as mild (35%), moderate (40.8%), and severe (24.3%) were included in the study. Monocytes from all COVID-19 patients were CD16+ pro-inflammatory monocytes. Neutrophils were mature and functional. No defect has been found in ROS production of monocytes and neutrophils as well as no defect in their apoptosis. As bridging cells of the innate and adaptive immune system; the percentage of NK cells was in normal range whereas the percentages of CD3-CD8+CD56+ innate lymphoid and CD3+CD56+ NK like T cells were found to be high in the severe cases of COVID-19. Although absolute numbers of all lymphocyte subsets were low and showed a tendency for a gradual decrease in accord with the disease progression, in all COVID-19 patients, the lymphocyte subset with the most decreased absolute number was B lymphocytes, followed by CD4 + T cells in the severe cases. The percentages of suppressive, CD3+CD4-CD8-; HLA-DR+CD3+ and CD28-CD8+ cells were found to be significantly increased. Importantly, we demonstrated spontaneous caspase-3 activation and increased lymphocyte apoptosis. Altogether our data suggest that SARS-CoV- 2 primarily affects lymphocytes not innate cells. So that, it may interrupt the cross-talk between adaptive and innate immune systems.

T cell maturation is significantly affected by SARS‐CoV‐2 infection

“…An increase in the percentage of CD28 neg T cells is observed in the elderly as well as in patients with autoimmune diseases and malignancies [36][37][38]. Although other studies cite an increase of CD28 neg T cells-especially with respect to CD8 + T lymphocytes-in severe and critically ill COVID-19 patients [23,26,[39][40][41][42], in this study, a reduction in CD28 neg T cells was observed both in the CD4 + and CD8 + cell compartment. These values did not recover 2 months after diagnosis and remained at much lower counts when compared to the control group.…”

Immune Response to COVID-19

“…In addition, cytokines can generate a systemic effect, resulting in damage to other organs (kidney, liver, spleen, among others) [20]. An increase in circulating pro-inflammatory monocytes and nonclassical monocytes are commonly observed in COVID-19 patients [21,22].…”

Issue Highlights—March 2022

“…As we begin a third year of the global SARS‐CoV‐2 pandemic, we continue to learn about host immune responses to the virus (Saksena & Chattopadhyay, 2021). Ekşioğlu‐Demiralp and colleagues have assessed a variety of phenotypic and functional properties of lymphocytes, monocytes, and neutrophils in a series of 103 SARS‐CoV‐2 patients categorized on the basis of disease severity (Ekşioğlu‐Demiralp et al, 2022). Among their many observations, the authors report significantly increased baseline activation (as assessed by CD69 expression) among CD4+ and CD8+ T cells in patients with severe compared with mild disease (Ekşioğlu‐Demiralp et al, 2022).…”

“…Ekşioğlu‐Demiralp and colleagues have assessed a variety of phenotypic and functional properties of lymphocytes, monocytes, and neutrophils in a series of 103 SARS‐CoV‐2 patients categorized on the basis of disease severity (Ekşioğlu‐Demiralp et al, 2022). Among their many observations, the authors report significantly increased baseline activation (as assessed by CD69 expression) among CD4+ and CD8+ T cells in patients with severe compared with mild disease (Ekşioğlu‐Demiralp et al, 2022). Huang and colleagues report increased co‐expression of TOX (a transcription factor implicated in promoting CD8+ T‐cell exhaustion) with the immunomodulatory receptors, PD‐1 and TIM‐3, and with CD244 (whose expression has been implicated in maintaining an exhausted T‐cell phenotype (Agresta et al, 2018) in the CD4+ and CD8+ T cells of patients with AML compared with healthy controls (Huang et al, 2022).…”