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Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell 2020 ; 183 (4): 982-995.e14 Nephropedia Template TP
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Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C) #MMPMID32991843
Gruber CN; Patel RS; Trachtman R; Lepow L; Amanat F; Krammer F; Wilson KM; Onel K; Geanon D; Tuballes K; Patel M; Mouskas K; O'Donnell T; Merritt E; Simons NW; Barcessat V; Del Valle DM; Udondem S; Kang G; Gangadharan S; Ofori-Amanfo G; Laserson U; Rahman A; Kim-Schulze S; Charney AW; Gnjatic S; Gelb BD; Merad M; Bogunovic D
Cell 2020[Nov]; 183 (4): 982-995.e14 PMID32991843show ga
Initially, children were thought to be spared from disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, a month into the epidemic, a novel multisystem inflammatory syndrome in children (MIS-C) emerged. Herein, we report on the immune profiles of nine MIS-C cases. All MIS-C patients had evidence of prior SARS-CoV-2 exposure, mounting an antibody response with intact neutralization capability. Cytokine profiling 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, and CCL28). Immunophenotyping of peripheral blood revealed reductions of non-classical monocytes, and subsets of NK and T lymphocytes, suggesting extravasation to affected tissues. Finally, profiling the autoantigen reactivity of MIS-C plasma 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-IL-6R antibody and/or IVIG, which led to rapid disease resolution.