An excellent new study by @BrodinPetter’s team on the differences between MIS-C and Kawasaki disease. This is incredibly timely and informative. Here are a couple of highlights. (1/)

https://www.cell.com/cell/fulltext/S0092-8674(20)31157-0">https://www.cell.com/cell/full... https://twitter.com/brodinpetter/status/1302634319345786881">https://twitter.com/brodinpet...

While there are some common features, MIS-C and Kawasaki disease differ in important areas. Non-overlapping symptoms and organ involvement, as well as the age group affected. Age in months in this study of MIS-C patients, 106 (71.1 - 165.4), and Kawasaki 24.5 (15.8 - 41.8). (2/)

Kawasaki disease patients have much higher levels of cytokines, IL-6, IL-17A and chemokine CXCL10, than either COVID-19 or MIS-C patients. (3/)

Notably, MIS-C patients did not have antibodies to other human coronaviruses, unlike COVID or Kawasaki patients (or healthy controls). Could this hCoV-naive state contribute to MIS-C development? (4/)

The most intriguing is the comparison of autoantibodies. MIS-C patients have higher levels of antibodies to MAP2K2 and to Casein kinase family members https://abs.twimg.com/emoji/v2/... draggable="false" alt="👇🏽" title="Rückhand Zeigefinger nach unten (mittlerer Hautton)" aria-label="Emoji: Rückhand Zeigefinger nach unten (mittlerer Hautton)"> On the other hand, Kawasaki patients had https://abs.twimg.com/emoji/v2/... draggable="false" alt="⬆️" title="Pfeil nach oben" aria-label="Emoji: Pfeil nach oben"> autoantibody against EDIL3. (5/)

This study begins to unravel the pathophysiology of MIS-C. Very curious to see if the autoantibodies are found in various tissues and induce leukocyte activation or complement fixation. (End)