A team of researchers from Mount Sinai claimed to have discovered an “important clue” behind a rare, potentially serious coronavirus-related inflammatory illness in children, called MIS-C.
MIS-C, which typically arises several weeks after a 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) states on its webpage.
As of July 30, the CDC noted over 4,400 reported cases of MIS-C, and at least 37 deaths.
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The latest findings published Wednesday in the Nature Communications journal stemmed from sequencing of blood samples which indicated a downregulation of so-called natural killer (NK) cells and an “exhausted” T cell subtype (CD8+), believed to contribute to the harmful bodily inflammation MIS-C patients can experience in the weeks following initial COVID-19 infection.
CD8+ T cells have previously been shown to enter a state of “exhaustion” upon persistent exposure to pathogens, thereby reducing their effectiveness, according to a news release.
Mount Sinai Hospital and School of Medicine dubbed the findings “a significant step in providing the field with new exploratory pathways involving complex networks and subnetworks of genes,” according to the news release posted to EurekAlert.org on Wednesday.
“Our study implicated T cell exhaustion in MIS-C patients as one of the potential drivers of this disease, suggesting that an increase in both NK cells and circulating exhausted CD8+ T cells may improve inflammatory disease symptoms,” lead co-author Noam Beckmann, PhD, assistant professor of genetics and genomic sciences at the Icahn School of Medicine at Mount Sinai, said in the release. “Additionally, we found nine key regulators of this network known to have associations with NK cell and exhausted CD8+ T cell functionality.”
Beckmann added that one regulator, TBX21, serves as a “promising therapeutic target” due to the role it plays as “a master coordinator of the transition of CD8+ T cells from effective to exhausted.”
