About: Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C)

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C)
Creator	Krammer, Florian Merad, Miriam Rahman, Adeeb Bogunovic, Dusan Amanat, Fatima Barcessat, Vanessa Charney, Alexander Gangadharan, Sandeep Geanon, Daniel Gelb, Bruce Gnjatic, Sacha Gruber, Conor Kang, Gurpawan Kim-Schulze, Seunghee Lepow, Lauren Mouskas, Konstantinos Ofori-Amanfo, George Onel, Kenan Patel, Manishkumar Patel, Roosheel Simons, Nicole Trachman, Rebecca Tuballes, Kevin Udondem, Samantha Valle, Diane Wilson, Karen
source	MedRxiv; Medline; PMC
abstract	Initially, the global outbreak of COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spared children from severe disease. However, after the initial wave of infections, clusters of a novel hyperinflammatory disease have been reported in regions with ongoing SARS-CoV-2 epidemics. While the characteristic clinical features are becoming clear, the pathophysiology remains unknown. Herein, we report on the immune profiles of eight Multisystem Inflammatory Syndrome in Children (MIS-C) cases. We document that all MIS-C patients had evidence of prior SARS-CoV-2 exposure, mounting an antibody response with normal isotype-switching and neutralization capability. We further profiled the secreted immune response by high-dimensional cytokine assays, which identified elevated signatures of inflammation (IL-18 and IL-6), lymphocytic and myeloid chemotaxis and activation (CCL3, CCL4, and CDCP1) and mucosal immune dysregulation (IL-17A, CCL20, CCL28). Mass cytometry immunophenotyping of peripheral blood revealed reductions of mDC1 and non-classical monocytes, as well as both NK- and T- lymphocytes, suggesting extravasation to affected tissues. Markers of activated myeloid function were also evident, including upregulation of ICAM1 and FcγR1 in neutrophil and non-classical monocytes, well-documented markers in autoinflammation and autoimmunity that indicate enhanced antigen presentation and Fc-mediated responses. Finally, to assess the role for autoimmunity secondary to infection, we profiled the auto-antigen reactivity of MIS-C plasma, which revealed both known disease-associated autoantibodies (anti-La) and novel candidates that recognize endothelial, gastrointestinal and immune-cell antigens. All patients were treated with anti-IL6R antibody or IVIG, which led to rapid disease resolution tracking with normalization of inflammatory markers.
has issue date	2020-07-06(xsd:dateTime)
bibo:doi	10.1101/2020.07.04.20142752
bibo:pmid	32676612
has license	no-cc
sha1sum (hex)	381042b486207b5f00f979001e91721d2c72e93c
schema:url	https://doi.org/10.1101/2020.07.04.20142752
resource representing a document's title	Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C)
has PubMed Central identifier	PMC7359537
has PubMed identifier	32676612
schema:publication	medRxiv : the preprint server for health sciences
resource representing a document's body	covid:381042b486207b5f00f979001e91721d2c72e93c#body_text
is schema:about of	named entity 'While' named entity 'response' named entity 'SARS-CoV-2' named entity 'lymphocytic' named entity 'profiles' named entity 'disease' named entity 'high-dimensional' named entity 'peripheral blood' named entity 'clusters' named entity 'secreted' named entity 'prior' named entity 'monocytes' named entity 'SARS-CoV-2' named entity 'cytokine' named entity 'global outbreak' named entity 'IL-6' named entity 'Antibody' named entity 'evidence' named entity 'mucosal' named entity 'mDC1' named entity 'SARS-CoV-2' named entity 'immune response' named entity 'immune dysregulation' named entity 'Mass cytometry' named entity 'extravasation' named entity 'IL-17A' named entity 'peripheral blood' named entity 'clinical features' named entity 'CCL3' named entity 'mounting' named entity 'infections' named entity 'global outbreak' named entity 'myeloid' named entity 'COVID' named entity 'CCL28' named entity 'MIS-C' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'antibody response' named entity 'IL-18' named entity 'immunophenotyping' named entity 'isotype' named entity 'CCL4' named entity 'MIS-C' named entity 'Inflammatory' named entity 'Multisystem' named entity 'Systemic Inflammation' named entity 'T-lymphocytes' named entity 'Multisystem' named entity 'inflammation' named entity 'Inflammatory' named entity 'epidemics' named entity 'MIS-C' covid:arg/381042b486207b5f00f979001e91721d2c72e93c named entity 'CCL20' named entity 'chemotaxis' named entity 'SARS-CoV-2'

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