Academic Journal

Natural Killer Cells Do Not Attenuate a Mouse-Adapted SARS-CoV-2-Induced Disease in Rag2−/− Mice

التفاصيل البيبلوغرافية
العنوان: Natural Killer Cells Do Not Attenuate a Mouse-Adapted SARS-CoV-2-Induced Disease in Rag2−/− Mice
المؤلفون: Calder R Ellsworth, Chenxiao Wang, Alexis R Katz, Zheng Chen, Mohammad Islamuddin, Haoran Yang, Sarah E Scheuermann, Kelly A Goff, Nicholas J Maness, Robert V Blair, Jay K Kolls, Xuebin Qin
المصدر: Viruses, Vol 16, Iss 4, p 611 (2024)
بيانات النشر: MDPI AG, 2024.
سنة النشر: 2024
المجموعة: LCC:Microbiology
مصطلحات موضوعية: SARS-CoV-2, MA30, COVID-19, T cells, B cells, NK cells, Microbiology, QR1-502
الوصف: This study investigates the roles of T, B, and Natural Killer (NK) cells in the pathogenesis of severe COVID-19, utilizing mouse-adapted SARS-CoV-2-MA30 (MA30). To evaluate this MA30 mouse model, we characterized MA30-infected C57BL/6 mice (B6) and compared them with SARS-CoV-2-WA1 (an original SARS-CoV-2 strain) infected K18-human ACE2 (K18-hACE2) mice. We found that the infected B6 mice developed severe peribronchial inflammation and rapid severe pulmonary edema, but less lung interstitial inflammation than the infected K18-hACE2 mice. These pathological findings recapitulate some pathological changes seen in severe COVID-19 patients. Using this MA30-infected mouse model, we further demonstrate that T and/or B cells are essential in mounting an effective immune response against SARS-CoV-2. This was evident as Rag2−/− showed heightened vulnerability to infection and inhibited viral clearance. Conversely, the depletion of NK cells did not significantly alter the disease course in Rag2−/− mice, underscoring the minimal role of NK cells in the acute phase of MA30-induced disease. Together, our results indicate that T and/or B cells, but not NK cells, mitigate MA30-induced disease in mice and the infected mouse model can be used for dissecting the pathogenesis and immunology of severe COVID-19.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1999-4915
Relation: https://www.mdpi.com/1999-4915/16/4/611; https://doaj.org/toc/1999-4915
DOI: 10.3390/v16040611
URL الوصول: https://doaj.org/article/18f1be7b00854737818d2aa9e4dc0ac8
رقم الانضمام: edsdoj.18f1be7b00854737818d2aa9e4dc0ac8
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19994915
DOI:10.3390/v16040611