Tumor Necrosis Factor Superfamily 14 drives the depletion of tissue-resident alveolar macrophages upon influenza A virus infection enabling the establishment of secondary pneumococcal pneumonia
dc.contributor.advisor | Herold, Susanne | |
dc.contributor.author | Malainou, Christina | |
dc.date.accessioned | 2023-11-14T13:58:31Z | |
dc.date.available | 2023-11-14T13:58:31Z | |
dc.date.issued | 2023 | |
dc.description.abstract | Tissue-resident alveolar macrophage (TR-AM) depletion is a key event upon influenza A virus (IAV)-induced pneumonia and one of the most important contributors to the establishment of post-viral pneumococcal pneumonia, a common complication of severe IAV infection. However, the mechanisms behind TR-AM death remain largely unknown. In the current study, the time frame, mechanisms, and related signaling pathways behind TR-AM loss after IAV infection were analyzed, proposing a novel mechanism for the preservation of the TR-AM pool through targeting of the tumor necrosis factor superfamily member 14 ligand-receptor axis. This offer a novel therapeutic approach both for IAV pneumonia and for secondary post-influenza pneumococcal infection. | de_DE |
dc.description.sponsorship | Deutsche Forschungsgemeinschaft (DFG); ROR-ID:018mejw64 | de_DE |
dc.identifier.uri | https://jlupub.ub.uni-giessen.de//handle/jlupub/18619 | |
dc.identifier.uri | http://dx.doi.org/10.22029/jlupub-17983 | |
dc.language.iso | en | de_DE |
dc.rights | In Copyright | * |
dc.rights.uri | http://rightsstatements.org/page/InC/1.0/ | * |
dc.subject | Influenza | de_DE |
dc.subject.ddc | ddc:610 | de_DE |
dc.title | Tumor Necrosis Factor Superfamily 14 drives the depletion of tissue-resident alveolar macrophages upon influenza A virus infection enabling the establishment of secondary pneumococcal pneumonia | de_DE |
dc.type | doctoralThesis | de_DE |
dcterms.dateAccepted | 2023-10-12 | |
local.affiliation | FB 11 - Medizin | de_DE |
thesis.level | thesis.doctoral | de_DE |
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