Academic Journal
SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway
| العنوان: | SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway |
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| المؤلفون: | Bortolotti D., Gentili V., Rizzo S., Rotola A., Rizzo R. |
| المساهمون: | Bortolotti, D., Gentili, V., Rizzo, S., Rotola, A., Rizzo, R. |
| سنة النشر: | 2020 |
| المجموعة: | Università degli Studi di Ferrara: CINECA IRIS |
| مصطلحات موضوعية: | SARS-CoV-2, NK cell, NKG2A, HLA-E, Cell Degranulation, Coronavirus Infections, Epithelial Cells, Histocompatibility Antigens Class I, Interferon-gamma, Lymphocyte Activation, Pandemic, K562 cells |
| الوصف: | Natural killer cells are important in the control of viral infections. However, the role of NK cells during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has previously not been identified. Peripheral blood NK cells from SARS-CoV and SARS-CoV-2 naïve subjects were evaluated for their activation, degranulation, and interferon-gamma expression in the presence of SARS-CoV and SARS-CoV-2 spike proteins. K562 and lung epithelial cells were transfected with spike proteins and co-cultured with NK cells. The analysis was performed by flow cytometry and immune fluorescence. SARS-CoV and SARS-CoV-2 spike proteins did not alter NK cell activation in a K562 in vitro model. On the contrary, SARS-CoV-2 spike 1 protein (SP1) intracellular expression by lung epithelial cells resulted in NK cell-reduced degranulation. Further experiments revealed a concomitant induction of HLA-E expression on the surface of lung epithelial cells and the recognition of an SP1-derived HLA-E-binding peptide. Simultaneously, there was increased modulation of the inhibitory receptor NKG2A/CD94 on NK cells when SP1 was expressed in lung epithelial cells. We ruled out the GATA3 transcription factor as being responsible for HLA-E increased levels and HLA-E/NKG2A interaction as implicated in NK cell exhaustion. We show for the first time that NK cells are affected by SP1 expression in lung epithelial cells via HLA-E/NKG2A interaction. The resulting NK cells' exhaustion might contribute to immunopathogenesis in SARS-CoV-2 infection. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | ELETTRONICO |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/32859121; info:eu-repo/semantics/altIdentifier/wos/WOS:000581800800001; volume:9; issue:9; firstpage:1975-1; lastpage:1975-15; numberofpages:15; journal:CELLS; http://hdl.handle.net/11392/2422040; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85090177634; https://www.mdpi.com/2073-4409/9/9/1975 |
| DOI: | 10.3390/cells9091975 |
| الاتاحة: | http://hdl.handle.net/11392/2422040 https://doi.org/10.3390/cells9091975 https://www.mdpi.com/2073-4409/9/9/1975 |
| Rights: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.923909D6 |
| قاعدة البيانات: | BASE |
| DOI: | 10.3390/cells9091975 |
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