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A team of researchers from Mount Sinai claimed to have found an “important clue” behind a rare and potentially serious inflammatory disease linked to coronavirus in children, called MIS-C.
MIS-C, which typically occurs several weeks after COVID-19 illness or contact with someone with COVID-19, can lead to organ damage due to a hyperinflammatory response. MIS-C can cause inflammation in one or more organ systems, including the heart, lungs, kidneys, gastrointestinal tract, brain, and / or skin. The cause of MIS-C is unknown, the Centers for Disease Control and Prevention (CDC) says on its webpage.
As of July 30, the CDC had noted more than 4,400 reported cases of MIS-C and at least 37 deaths.
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The latest findings published Wednesday in the journal Nature Communications stem from the sequencing of blood samples that indicated downregulation of so-called natural killer (NK) cells and an “depleted” T cell subtype (CD8 +), believed to contribute to the harmful body inflammation. MIS-C patients may suffer within weeks of initial infection with COVID-19.
CD8 + T cells have previously been shown to enter a “depleted” state upon persistent exposure to pathogens, thereby reducing their effectiveness, according to a press release.
Mount Sinai Hospital and School of Medicine called the findings “an important step in providing the field with new exploratory pathways involving complex arrays and subnetworks of genes,” according to the press release on EurekAlert on Wednesday. .org.
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“Our study implicated T cell depletion in MIS-C patients as one of the potential drivers of this disease, suggesting that an increase in circulating NK cells and depleted CD8 + T cells may improve symptoms of the disease. inflammatory disease, “co-lead author Noam Beckmann, PhD, assistant professor of genetics and genomic sciences at Icahn School of Medicine at Mount Sinai, said in the statement. “In addition, we have found nine key regulators of this network known to have associations with NK cells and to deplete the functionality of CD8 + T cells.”
Beckmann added that a regulator, TBX21, serves as a “promising therapeutic target” because of its role as “the primary coordinator of the transition of CD8 + T cells from efficient to exhausted”.
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