INTRODUCTION
The SARS-CoV-2 virus, originating from Wuhan, China since December 2019, causing a worldwide pandemic is a positive-sense single-stranded RNA virus (1, 2). The disease caused was called Coronavirus disease 2019 (COVID-19).
COVID-19 disease can progress mildly (81%), moderate to severe (14%) according to pulmonary involvement, and critical (5%) with multiple organ failure (3). The recent mortality rate has reached 6.3%, although it varies with age, gender, occupational group, and the presence of comorbidities such as diabetes, hypertension (4-6).
First-line defense against intracellular invaders such as viruses starts with innate immune cells including monocytes, macrophages, neutrophils. Activation of monocytes, macrophages, and bystanders, bridging dendritic cells by pattern recognition receptors results in releasing of proinflammatory cytokines such as IL-1, IL-18, IL-33, and IL-6. Those cytokines activate Natural Killer (NK) cells. NK activation is critical for viral defense because of both their cellular cytotoxic function as well as their cytokine release in particular interferon-gamma that activates both B and T cells (7). Adaptive activation is a requirement for both eliminating invaders, constructing a proper immune memory, and also for limiting innate activation. Studies in T cell and RAG-1 deficient mice demonstrated that lack of lymphocytes resulted in cytokine storm syndrome and death (8). Crosstalk between natural and adaptive immune systems constitutes our entire immune system, but every fine-tuned interaction is a target point for invaders.
The vicious circle of cytokine storm syndrome and hyperinflammation seen in COVID-19 deteriorate patients rapidly and mortality rate increases in this group due to respiratory failure (9). One of the main reasons for the rapid deterioration of COVID-19 patients is hyper inflammation and cytokine storm syndrome (10, 11).  Studies show that SARS-COV2 uses strategies to inhibit the interferon signaling pathway. Thus it can be considered that it silences adaptive activation (12).
Although what is known about immune pathogenesis of the disease is very limited, lymphopenia, the change of neutrophil/lymphocyte ratio in favor of neutrophils, increased level of LDH, CRP and ferritin vary in proportion with the severity of the disease and are used in the follow-up of the disease (13-15). In the autopsies of the individuals who died due to Covid-19, neutrophil, and monocyte/macrophage infiltration and few helper T cells were detected in their lungs (16, 17). It is noteworthy that the natural killer (NK) and CD8+ cytotoxic T cells, which are of primary importance in the fight against viral infection, are not present in the field (18).
Immune profiles of individuals with Covid-19 disease should be examined and be informed more to establish explanatory immune hypotheses on this disease. In this cross-sectional study, we aimed to investigate peripheral innate and adaptive cells, burst and phagocytosis functions of monocyte and neutrophils and lymphocyte apoptosis of patients with COVID-19, We also examined any association of these immune parameters with severity of the disease. The data compared against the normal values ​​of the individuals used as a healthy control group in previous studies of the group or the defined normal values ​​of the subgroups.
Delineation of the phenotypic and functional impairments created by the SARS-CoV-2 virus in the cells of the innate and adaptive immune systems will help to better recognize the virus and develop treatment and prevention strategies.