A recent study published in the journal Nature evaluated differential autoreactivity to human and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proteomes in SARS-CoV-2-infected children with and without multisystem inflammatory syndrome (MIS-C). SARS-CoV-2 typically causes mild illness in children but can lead to MIS-C, a rare, life-threatening condition. This condition presents with a complex and heterogeneous clinical profile, making it particularly challenging to understand.
MIS-C is characterized by a distinct inflammatory signature indicative of altered innate immunity. In particular, dysregulation of the mitochondrial antiviral signaling (MAVS) protein pathway has been highlighted in MIS-C pathology, contributing to the unique inflammatory profile observed in these patients. Besides, aberrant adaptive immunity is also involved.
Various MIS-C-associated autoantibodies have been reported. Further, T cell signatures are also associated with MIS-C development, accompanied by autoimmune-related B cell expansions. However, pathological links between SARS-CoV-2 and MIS-C are unclear.
The study’s rigorous design involved comprehensive evaluations of proteome-wide autoantibody profiles, leveraging a larger cohort size than previous studies to ensure robustness and minimize spurious associations. Study: Molecular mimicry in multisystem inflammatory syndrome in children . Image Credit: NIAID The study and findings The present study evaluated d.