アメリカ生活が長く、もはや日本語を話す方が下手になったと、おっしゃってました。
In this study, we enrolled COVID+ patients and analyzed their immune responses and viral load over the course of their hospital stay. We also compared samples from COVID- healthy health care workers (HCWs) as comparison. (2/n) pic.twitter.com/aZoT1emy1I
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
The serum cytokines indicate the activation of inflammasomes based on elevated cytokines IL-18 and IL-1b, as well as IL-6. For more on the #Inflammasome and #COVID19, see review by @jeremymmunology @MiyuMoriyama (4/n)https://t.co/dV4qan1o1u
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
In severe #COVID19, we find all cytokine types being elevated overtime in patients. Even eosinophils and IgE which are good for expelling worms and not for viral defence became elevated in severe cases. (6/n) pic.twitter.com/UBqk3sQcrV
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
Is it that patients with severe disease fail to produce antiviral interferons? No! They are making more interferons and other innate cytokines in response to viral load, suggesting that these #IFNs are not able to control virus in patients. (8/n) pic.twitter.com/yhypndjloy
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
These data build nicely on others’ seminal work @Lo_Zanzi and Peng Hong showing the detrimental effects of late IFNs in #COVID19. (10/n)https://t.co/etjjT97ErShttps://t.co/vLJUX139HO
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
We then asked if we take all patients and all time points and group them based on their cytokine profile, what do we get? We got a remarkably similar clustering based on almost identical immune signatures. (12/n) pic.twitter.com/qhTxrem7wx
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
How can we use these insights for future treatment? First, we found biomarkers for mortality. An amazing work by @mariasundaram @Muhellingson @SaadOmer3. These biomarkers can be a useful prognostic tool for better targeted therapy. (14/n) pic.twitter.com/qzAZFNMp4P
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
Lastly, this work is a huge collaboration across @YaleIBIO @YaleMed @YNHH @YaleSPH @YaleIDFellows @YaleCancer @YaleNursing @YalePCCSM @YaleGH @yale_Labmed @RockefellerUniv @HHMINEWS. Enormously rewarding to learn from our patients -my first translational immunology paper 🙏🏼 (end) pic.twitter.com/AdffclPc2D
— Prof. Akiko Iwasaki (@VirusesImmunity) July 27, 2020
ヒトACE2を発現するように仕立てたマウスの新型コロナウイルス感染実験によると1型インターフェロンはウイルスの複製を阻止せず、肺に炎症性細胞をより集まらせる。研究を率いたエール大学のAkiko Iwasaki(岩崎明子)氏は早めのインターフェロン投与が肝心だと言っている。https://t.co/wySKQWuTUh
— biotoday (@BioTodaySuppl) August 6, 2020
