Extracellular Vesicles from Apoptotic Cells Promote TGFβ Production in Macrophages and Suppress Experimental Colitis
| Autor: | Shimpei Kasagi, Peter Zanvit, Eric Tu, Hua Chen, Nathan Goldberg, Dunfang Zhang, Wenwen Jin, Cheryl Chia, Wanjun Chen, Ruiqing Wu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
lcsh:Medicine Apoptosis Phosphatidylserines Jurkat cells Article 03 medical and health sciences chemistry.chemical_compound Extracellular Vesicles Jurkat Cells Mice 0302 clinical medicine Mediator Immune system Transforming Growth Factor beta Macrophage Animals Humans RNA Small Interfering lcsh:Science Transcription factor Homeodomain Proteins Mice Knockout Mice Inbred BALB C Multidisciplinary Thymocytes Chemistry Macrophages lcsh:R Forkhead Box Protein O3 Phosphatidylserine Colitis Cell biology Mice Inbred C57BL Disease Models Animal 030104 developmental biology Gamma Rays FOXO3 lcsh:Q RNA Interference 030217 neurology & neurosurgery |
| Zdroj: | Scientific Reports Scientific Reports, Vol 9, Iss 1, Pp 1-10 (2019) |
| ISSN: | 2045-2322 |
| Popis: | The clearance of apoptotic cells is an essential process to maintain homeostasis of immune system, which is regulated by immunoregulatory cytokines such as TGFβ. We show here that Extracellular Vesicles (EVs) were highly released from apoptotic cells, and contributed to macrophage production of TGFβ in vitro and in vivo. We further elucidated mechanistically that phosphatidylserine in EVs was a key triggering-factor, and transcription factor FOXO3 was a critical mediator for apoptotic EV-induced TGFβ in macrophages. Importantly, we found that macrophages pre-exposed to EVs exhibited an anti-inflammatory phenotype. More strikingly, administration of EVs in vivo promotes Tregs differentiation and suppresses Th1 cell response, and ameliorates experimental colitis. Thus, apoptotic-EV-based treatment might be a promising therapeutic approach for human autoimmune disease. |
| Databáze: | OpenAIRE |
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