{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bonam SR"],"funding":["Agence Nationale de la Recherche"],"pagination":["838448"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8907115"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Basophils play a key role in the orientation of immune responses. Though the interaction of SARS-CoV-2 with various immune cells has been relatively well studied, the response of basophils to this pandemic virus is not characterized yet. In this study, we report that SARS-CoV-2 induces cytokine responses and in particular IL-13, in both resting and IL-3 primed basophils. The response was prominent under IL-3 primed condition. However, either SARS-CoV-2 or SARS-CoV-2-infected epithelial cells did not alter the expression of surface markers associated with the activation of basophils, such as CD69, CD13 and/or degranulation marker CD107a. We also validate that human basophils are not permissive to SARS-CoV-2 replication. Though increased expression of immune checkpoint molecule PD-L1 has been reported on the basophils from COVID-19 patients, we observed that SARS-CoV-2 does not induce PD-L1 on the basophils. Our data suggest that basophil cytokine responses to SARS-CoV-2 might help in reducing the inflammation and also to promote antibody responses to the virus."],"journal":["Frontiers in immunology"],"pubmed_title":["SARS-CoV-2 Induces Cytokine Responses in Human Basophils."],"pmcid":["PMC8907115"],"funding_grant_id":["ANR-20-COVI-0093-COVIMUNE"],"pubmed_authors":["Sakuntabhai A","Chauvin C","Mathew MJ","Bayry J","Bonam SR","Levillayer L"],"additional_accession":[]},"is_claimable":false,"name":"SARS-CoV-2 Induces Cytokine Responses in Human Basophils.","description":"Basophils play a key role in the orientation of immune responses. Though the interaction of SARS-CoV-2 with various immune cells has been relatively well studied, the response of basophils to this pandemic virus is not characterized yet. In this study, we report that SARS-CoV-2 induces cytokine responses and in particular IL-13, in both resting and IL-3 primed basophils. The response was prominent under IL-3 primed condition. However, either SARS-CoV-2 or SARS-CoV-2-infected epithelial cells did not alter the expression of surface markers associated with the activation of basophils, such as CD69, CD13 and/or degranulation marker CD107a. We also validate that human basophils are not permissive to SARS-CoV-2 replication. Though increased expression of immune checkpoint molecule PD-L1 has been reported on the basophils from COVID-19 patients, we observed that SARS-CoV-2 does not induce PD-L1 on the basophils. Our data suggest that basophil cytokine responses to SARS-CoV-2 might help in reducing the inflammation and also to promote antibody responses to the virus.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2025-04-04T07:54:57.035Z","creation":"2025-04-04T07:54:57.035Z"},"accession":"S-EPMC8907115","cross_references":{"pubmed":["35280992"],"doi":["10.3389/fimmu.2022.838448"]}}