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Mononuclear phagocytes, particularly those in the liver and spleen, restrict bacterial replication in the initial phase of a primary invasive infection. Specific elements of both innate and adaptive immunity are needed to control Salmonella and other intracellular pathogens. Typhimurium provides a useful model of immunity to this bacterium and others that colonize macrophages ( Chatfield et al., 1992 Conlan, 1997 Richter-Dahlfors et al., 1997 Mastroeni et al., 2000 Vazquez-Torres et al., 2000a, 2004 Burton et al., 2014). Our understanding of the immune response to such common and serious pathogens remains incomplete, though infection of mice with S. Both can be fatal, particularly in immunocompromised hosts. For example, specific serovars of Salmonella such as typhi and paratyphi cause typhoid fever (enteric fever), whereas nontyphi Salmonella can also cause invasive systemic infection ( Dougan et al., 2011 Gilchrist et al., 2015). Infectious diseases cause major morbidity and mortality worldwide. We thus describe the key role of the previously uncharacterized protein Eros in host defense. Eros is an ortholog of the plant protein Ycf4, which is necessary for expression of proteins of the photosynthetic photosystem 1 complex, itself also an NADPH oxio-reductase. Eros also contributes to the formation of neutrophil extracellular traps (NETS) and impacts on the immune response to melanoma metastases. Consequently, Eros-deficient mice quickly succumb to infection.
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Eros is required for expression of the NADPH oxidase components, gp91 phox and p22 phox. We describe Eros (essential for reactive oxygen species), a protein encoded by the previously undefined mouse gene bc017643, and show that it is essential for host defense via the phagocyte NAPDH oxidase. Deficiency of either subunit leads to severe immunodeficiency. The transfer of electrons to oxygen is mediated by a membrane-bound heterodimer, comprising gp91 phox and p22 phox subunits. PMID: 34846101 | DOI: 10.1002/cyto.b.The phagocyte respiratory burst is crucial for innate immunity.
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Therefore, this may interrupt the crosstalk between the adaptive and innate immune systems. The increased baseline activation of Caspase-3 could make the COVID-19 lymphocytes more vulnerable to cell death. Importantly, we demonstrated the increased baseline activation of caspase-3 and increased lymphocyte apoptosis.ĬONCLUSION: We suggest that SARS-CoV-2 primarily affects the lymphocytes and not the innate cells. The percentages of double-negative T cells HLA-DR + CD3 + and CD28 – CD8 + subsets were found to be significantly increased. Although the absolute numbers of all lymphocyte subsets were low and showed a tendency for a gradual decrease in accordance with the disease progression, the most decreased absolute number was that of B lymphocytes, followed by CD4 + T cells in the severe cases. The percentage of natural killer cells was in the normal range, whereas the percentages of CD8 + NK and CD56 + T lymphocytes were found to be high (p < 0.01). No defect was found in the reactive oxygen species production and their apoptosis. Neutrophils were mature and functional, although a decline of their CD10 and CD16 was observed (p < 0.01). RESULTS: Monocytes were CD16 + pro-inflammatory monocytes and tended to shed their HLA-DR, especially in severe cases (p < 0.01). One hundred and three patients with COVID-19 were grouped according to their clinical features into the categories of mild (35%), moderate (40.8%), and severe (24.3%). METHODS: We studied phenotypic features of innate and adaptive immune cells, oxidative burst, phagocytosis, and apoptosis. Online ahead of print.īACKGROUND: A better understanding of innate and adaptive cells in COVID-19 is necessary for the development of effective treatment methods and vaccines.