Journal
SCIENCE IMMUNOLOGY
Volume 6, Issue 57, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.abf7570
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Funding
- NIH [K08 AI136660, AI105343, AI082630, HL137006, HL137915, CA230157, T32 CA009140, T32-AI-007324, CA234842, HL143613, R01AI121250, K08AI135091, R01CA193776]
- University of Pennsylvania Institute for Immunology Glick COVID-19 research award
- Allen Institute for Immunology
- Cancer Research Institute-Mark Foundation Fellowship
- Burroughs Wellcome Fund Career Award for Medical Scientists
- Leukemia and Lymphoma Society
- Alex's Lemonade Stand Foundation for Childhood Cancer
- CHOP Frontiers Program Immune Dysregulation Team
- Athersys, Inc.
- Marcus Foundation for Research
- Parker Institute for Cancer Immunotherapy
- Children's Hospital of Philadelphia, Research Institute American Association of Allergy, Asthma and Immunology Foundation Faculty Development Award Burroughs Wellcome Fund Career Awards for Medical Scientists
- Biomarck, Inc.
- University of Pennsylvania Institute for Translational Medicine and Therapeutics
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Pediatric COVID-19 following SARS-CoV-2 infection in children is generally less severe than in adults, but the subset of children with MIS-C exhibit immune features similar to severely ill adults and vascular complications. MIS-C patients show robust activation of T cells and vascular patrolling cells, correlating with the use of vasoactive medication. Unlike pediatric COVID-19 patients with ARDS, MIS-C patients display clinical improvement over time along with decreasing immune activation.
Pediatric COVID-19 following SARS-CoV-2 infection is associated with fewer hospitalizations and often milder disease than in adults. A subset of children, however, present with Multisystem Inflammatory Syndrome in Children (MIS-C) that can lead to vascular complications and shock, but rarely death. The immune features of MIS-C compared to pediatric COVID-19 or adult disease remain poorly understood. We analyzed peripheral blood immune responses in hospitalized SARS-CoV-2 infected pediatric patients (pediatric COVID-19) and patients with MIS-C. MIS-C patients had patterns of T cell-biased lymphopenia and T cell activation similar to severely ill adults, and all patients with MIS-C had SARS-CoV-2 spikespecific antibodies at admission. A distinct feature of MIS-C patients was robust activation of vascular patrolling CX3CR1+ CD8+ T cells that correlated with the use of vasoactive medication. Finally, whereas pediatric COVID-19 patients with acute respiratory distress syndrome (ARDS) had sustained immune activation, MIS-C patients displayed clinical improvement over time, concomitant with decreasing immune activation. Thus, non-MIS-C versus MIS-C SARS-CoV-2 associated illnesses are characterized by divergent immune signatures that are temporally distinct from one another and implicate CD8+ T cells in the clinical presentation and trajectory of MIS-C.
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