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10.1101/2021.04.13.21255439

http://scihub22266oqcxt.onion/10.1101/2021.04.13.21255439
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33907759!8077582!33907759
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suck abstract from ncbi


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pmid33907759      medRxiv 2021 ; ä (ä): ä
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  • Proteomic Profiling of MIS-C Patients Reveals Heterogeneity Relating to Interferon Gamma Dysregulation and Vascular Endothelial Dysfunction #MMPMID33907759
  • Diorio C; Shraim R; Vella LA; Giles JR; Baxter AE; Oldridge DA; Canna SW; Henrickson SE; McNerney KO; Balamuth F; Burudpakdee C; Lee J; Leng T; Farrell A; Lambert MP; Sullivan KE; John Wherry E; Teachey DT; Bassiri H; Behrens EM
  • medRxiv 2021[Apr]; ä (ä): ä PMID33907759show ga
  • Multi-system Inflammatory Syndrome in Children (MIS-C) is a major complication of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pandemic in pediatric patients. Weeks after an often mild or asymptomatic initial infection with SARS-CoV-2 children may present with a severe shock-like picture and marked inflammation. Children with MIS-C present with varying degrees of cardiovascular and hyperinflammatory symptoms. We performed a comprehensive analysis of the plasma proteome of more than 1400 proteins in children with SARS-CoV-2. We hypothesized that the proteome would reflect heterogeneity in hyperinflammation and vascular injury, and further identify pathogenic mediators of disease. Protein signatures demonstrated overlap between MIS-C, and the inflammatory syndromes macrophage activation syndrome (MAS) and thrombotic microangiopathy (TMA). We demonstrate that PLA2G2A is a key marker of MIS-C that associates with TMA. We found that IFNgamma responses are dysregulated in MIS-C patients, and that IFNgamma levels delineate clinical heterogeneity.
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