SARS-CoV-2-related MIS-C: A key to the viral and genetic causes of kawasaki disease?
Göster/ Aç
Erişim
info:eu-repo/semantics/openAccessAttribution-NonCommercial-ShareAlike 4.0 Internationalhttps://creativecommons.org/licenses/by-nc-sa/4.0/Tarih
2021Yazar
Sancho-Shimizu, VanessaBrodin, Petter
Cobat, Aurelie
Biggs, Catherine M.
Toubiana, Julie
Lucas, Carrie L.
Henrickson, Sarah E.
Belot, Alexandre
Tangye, Stuart G.
Milner, Joshua D.
Levin, Michael
Abel, Laurent
Bogunovic, Dusan
Casanova, Jean-Laurent
Zhang, Shen-Ying
Nepesov, Serdar
Üst veri
Tüm öğe kaydını gösterKünye
Sancho-Shimizu, V., Brodin, P., Cobat, A., Biggs, C. M., Toubiana, J., Lucas, C. L. ... Nepesov, S. (2021). SARS-CoV-2-related MIS-C: A key to the viral and genetic causes of kawasaki disease? Journal of Experimental Medicine, 218(6). https://dx.doi.org/10.1084/jem.20210446Özet
Multisystem inflammatory syndrome in children (MIS-C) emerged in April 2020 in communities with high COVID-19 rates. This new condition is heterogenous but resembles Kawasaki disease (KD), a well-known but poorly understood and clinically heterogenous pediatric inflammatory condition for which weak associations have been found with a myriad of viral illnesses. Epidemiological data clearly indicate that SARS-CoV-2 is the trigger for MIS-C, which typically occurs about 1 mo after infection. These findings support the hypothesis of viral triggers for the various forms of classic KD. We further suggest that rare inborn errors of immunity (IEIs) altering the immune response to SARS-CoV-2 may underlie the pathogenesis of MIS-C in some children. The discovery of monogenic IEIs underlying MIS-C would shed light on its pathogenesis, paving the way for a new genetic approach to classic KD, revisited as a heterogeneous collection of IEIs to viruses.