Kemal Mese, Esther Maguilla Rosado, Carsten G K Lüder, Ahmed Sayed Abdel-Moneim, Patrick Jordan, Julian Schwanbeck, Oskar Bunz, Raimond Lugert, Wolfgang Bohne, Jian Gao, Anna Dudakova, Uwe Groß, Andreas E Zautner
{"title":"FcγRIIa 介导的 SARS-CoV-2 抗体依赖性吸收可增强单核细胞的 IL-6 表达。","authors":"Kemal Mese, Esther Maguilla Rosado, Carsten G K Lüder, Ahmed Sayed Abdel-Moneim, Patrick Jordan, Julian Schwanbeck, Oskar Bunz, Raimond Lugert, Wolfgang Bohne, Jian Gao, Anna Dudakova, Uwe Groß, Andreas E Zautner","doi":"10.1556/1886.2024.00109","DOIUrl":null,"url":null,"abstract":"<p><p>This work aimed to investigate interactions between antibody-opsonized SARS-CoV-2 and monocytes enriched from human peripheral blood mononuclear cells (PBMC) to determine whether antibody dependent enhancement might contribute to the pathophysiology of COVID-19. Pre-incubation of SARS-CoV-2 with sera from hospitalized COVID-19 patients led to significantly increased virus uptake and viral replication in monocytes. Remarkably, SARS-CoV-2 pre-incubated with sera from patients with severe COVID-19 but not those with mild disease or post vaccination strongly increased IL-6 secretion by monocytes. Antibody dependent viral uptake was partially inhibited by monoclonal anti-FcγRIIa antibody whereas IL-6 secretion was completely abolished. FcγRIIa preferentially binds IgG2, and sera from patients with severe COVID-19 contained lower IgG2 levels as compared to mild COVID-19 cases whereas IgG1 levels were increased. These data suggests that FcγRIIa-mediated binding of antibody-opsonized SARS-CoV-2 critically impacts monocytic inflammatory cytokine release and COVID-19 pathophysiology.</p>","PeriodicalId":93998,"journal":{"name":"European journal of microbiology & immunology","volume":" ","pages":"380-391"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"FcγRIIa-mediated antibody-dependent uptake of SARS-CoV-2 enhances IL-6 expression of monocytes.\",\"authors\":\"Kemal Mese, Esther Maguilla Rosado, Carsten G K Lüder, Ahmed Sayed Abdel-Moneim, Patrick Jordan, Julian Schwanbeck, Oskar Bunz, Raimond Lugert, Wolfgang Bohne, Jian Gao, Anna Dudakova, Uwe Groß, Andreas E Zautner\",\"doi\":\"10.1556/1886.2024.00109\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>This work aimed to investigate interactions between antibody-opsonized SARS-CoV-2 and monocytes enriched from human peripheral blood mononuclear cells (PBMC) to determine whether antibody dependent enhancement might contribute to the pathophysiology of COVID-19. Pre-incubation of SARS-CoV-2 with sera from hospitalized COVID-19 patients led to significantly increased virus uptake and viral replication in monocytes. Remarkably, SARS-CoV-2 pre-incubated with sera from patients with severe COVID-19 but not those with mild disease or post vaccination strongly increased IL-6 secretion by monocytes. Antibody dependent viral uptake was partially inhibited by monoclonal anti-FcγRIIa antibody whereas IL-6 secretion was completely abolished. FcγRIIa preferentially binds IgG2, and sera from patients with severe COVID-19 contained lower IgG2 levels as compared to mild COVID-19 cases whereas IgG1 levels were increased. These data suggests that FcγRIIa-mediated binding of antibody-opsonized SARS-CoV-2 critically impacts monocytic inflammatory cytokine release and COVID-19 pathophysiology.</p>\",\"PeriodicalId\":93998,\"journal\":{\"name\":\"European journal of microbiology & immunology\",\"volume\":\" \",\"pages\":\"380-391\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-12-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European journal of microbiology & immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1556/1886.2024.00109\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/12/18 0:00:00\",\"PubModel\":\"Print\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of microbiology & immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1556/1886.2024.00109","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/18 0:00:00","PubModel":"Print","JCR":"","JCRName":"","Score":null,"Total":0}
FcγRIIa-mediated antibody-dependent uptake of SARS-CoV-2 enhances IL-6 expression of monocytes.
This work aimed to investigate interactions between antibody-opsonized SARS-CoV-2 and monocytes enriched from human peripheral blood mononuclear cells (PBMC) to determine whether antibody dependent enhancement might contribute to the pathophysiology of COVID-19. Pre-incubation of SARS-CoV-2 with sera from hospitalized COVID-19 patients led to significantly increased virus uptake and viral replication in monocytes. Remarkably, SARS-CoV-2 pre-incubated with sera from patients with severe COVID-19 but not those with mild disease or post vaccination strongly increased IL-6 secretion by monocytes. Antibody dependent viral uptake was partially inhibited by monoclonal anti-FcγRIIa antibody whereas IL-6 secretion was completely abolished. FcγRIIa preferentially binds IgG2, and sera from patients with severe COVID-19 contained lower IgG2 levels as compared to mild COVID-19 cases whereas IgG1 levels were increased. These data suggests that FcγRIIa-mediated binding of antibody-opsonized SARS-CoV-2 critically impacts monocytic inflammatory cytokine release and COVID-19 pathophysiology.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
