![]() ![]() The exact pathogenesis of novel coronavirus pneumonia is not fully understood, although the secondary systemic immune cell inflammatory response and cytokine storm caused by SAR-Cov-2 have been recognized as an important cause of its high lethality. The pathological process of COVID-19 can be divided into three stages: (1) SARS-CoV-2 invasion and replication (2) immune response and cytokine storm (3) acute respiratory distress syndrome and multiple organ dysfunction syndromes. The most common clinical manifestations are fever, cough, shortness of breath, muscle aches, confusion, headache, sore throat, runny nose, chest pain, diarrhea, nausea, and vomiting. Patients with COVID-19 can be clinically classified into four categories: mild, common, severe, and critical. Since the start of this international public health emergency, there have been more than 400 million confirmed cases, with more than 6 million deaths worldwide. The aim of this review is to explore the potential value of the IL-33/immune cell pathway as a new target for early diagnosis, monitoring of severe cases, and clinical treatment of COVID-19.ĬOVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has a long incubation period and is highly contagious. In this review, we systematically discuss the biological properties of IL-33 under pathophysiological conditions and its regulation of immune cells, including neutrophils, innate lymphocytes (ILCs), dendritic cells, macrophages, CD4 + T cells, Th17/Treg cells, and CD8 + T cells, in COVID-19 phagocytosis. However, the effects of IL-33 in COVID-19 and the underlying mechanisms remain to be fully elucidated. Increased IL-33 levels in severe infections may result from an inflammatory storm caused by strong interactions between activated immune cells. Recent studies have shown that serum IL-33 is upregulated in COVID-19 patients and is strongly associated with poor outcomes. As an inflammatory storm factor, IL-33 is an alarmin cytokine, which plays an important role in cell damage or infection. Despite intensified efforts to clarify the immunopathology of COVID-19, the key factors and processes that trigger an inflammatory storm and lead to severe clinical outcomes in patients remain unclear. The present results provide a detailed comparison of human CD3(+)CD8(+)CD57(bright) CTLs and NK cells and suggest that analysis of CD57(bright) CTL function may prove useful in the diagnosis of primary immunodeficiencies including familial hemophagocytic lymphohistiocytosis.Since the start of COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), more than 6 million people have lost their lives worldwide directly or indirectly. Therefore, cytotoxic lymphocyte subsets have similar requirements for Munc13-4, syntaxin-11, and Munc18-2 in lytic granule exocytosis. In patients with biallelic mutations in UNC13D, STX11, or STXBP2 associated with familial hemophagocytic lymphohistiocytosis, CTL and NK cell degranulation were similarly impaired. Remarkably, the CTLs produced cytokines more rapidly and with greater frequency than NK cells. On stimulation, such CTLs degranulated more readily than other T-cell subsets, but had a propensity to degranulate that was similar to NK cells. Healthy adult peripheral blood CD3(+)CD8(+)CD57(bright) CTLs expressed more granzyme B but less perforin than CD3(-)CD56(dim) NK cells. We then compared CD3(+)CD8(+)CD57(bright) CTLs with NK cells. Analysis identified CD57(bright) expression as a reliable phenotype of granule marker-containing CTLs. In the present study, we first performed probability-state modeling of differentiation and lytic granule markers on CD8(+) T cells to enable the comparison of bona fide CTLs with NK cells. Cytotoxic lymphocytes, encompassing cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, kill pathogen-infected, neoplastic, or certain hematopoietic cells through the release of perforin-containing lytic granules. ![]()
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