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Article: Exosomes contribute to the transmission of anti-HIV activity from TLR3-activated brain microvascular endothelial cells to macrophages

TitleExosomes contribute to the transmission of anti-HIV activity from TLR3-activated brain microvascular endothelial cells to macrophages
Authors
KeywordsAntiviral
BBB
Exosomes
HBMECs
TLR3
Issue Date2016
Citation
Antiviral Research, 2016, v. 134, p. 167-171 How to Cite?
AbstractHuman brain microvascular endothelial cells (HBMECs), the major cell type in the blood-brain barrier (BBB), play a key role in maintaining brain homeostasis. However, their role in the BBB innate immunity against HIV invasion of the central nervous system (CNS) remains to be determined. Our early work showed that TLR3 signaling of HBMECs could produce the antiviral factors that inhibit HIV replication in macrophages. The present study examined whether exosomes from TLR3-activated HBMECs mediate the intercellular transfer of antiviral factors to macrophages. Primary human macrophages could take up exosomes from TLR3-activated HBMECs. HBMECs-derived exosomes contained multiple antiviral factors, including several key IFN-stimulated genes (ISGs; ISG15, ISG56, and Mx2) at mRNA and protein levels. The depletion of exosomes from TLR3-activated HBMECs culture supernatant diminished HBMECs-mediated anti-HIV activity in macrophages. In conclusion, we demonstrate that exosomes shed by HBMECs are able to transport the antiviral molecules to macrophages. This finding suggests the possibility that HIV nonpermissive BBB cells (HBMECs) can help to restore the antiviral state in HIV-infected macrophages, which may be a defense mechanism against HIV neuroinvasion.
Persistent Identifierhttp://hdl.handle.net/10722/321702
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.500
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSun, Li-
dc.contributor.authorWang, Xu-
dc.contributor.authorZhou, Yu-
dc.contributor.authorZhou, Run Hong-
dc.contributor.authorHo, Wen Zhe-
dc.contributor.authorLi, Jie Liang-
dc.date.accessioned2022-11-03T02:20:53Z-
dc.date.available2022-11-03T02:20:53Z-
dc.date.issued2016-
dc.identifier.citationAntiviral Research, 2016, v. 134, p. 167-171-
dc.identifier.issn0166-3542-
dc.identifier.urihttp://hdl.handle.net/10722/321702-
dc.description.abstractHuman brain microvascular endothelial cells (HBMECs), the major cell type in the blood-brain barrier (BBB), play a key role in maintaining brain homeostasis. However, their role in the BBB innate immunity against HIV invasion of the central nervous system (CNS) remains to be determined. Our early work showed that TLR3 signaling of HBMECs could produce the antiviral factors that inhibit HIV replication in macrophages. The present study examined whether exosomes from TLR3-activated HBMECs mediate the intercellular transfer of antiviral factors to macrophages. Primary human macrophages could take up exosomes from TLR3-activated HBMECs. HBMECs-derived exosomes contained multiple antiviral factors, including several key IFN-stimulated genes (ISGs; ISG15, ISG56, and Mx2) at mRNA and protein levels. The depletion of exosomes from TLR3-activated HBMECs culture supernatant diminished HBMECs-mediated anti-HIV activity in macrophages. In conclusion, we demonstrate that exosomes shed by HBMECs are able to transport the antiviral molecules to macrophages. This finding suggests the possibility that HIV nonpermissive BBB cells (HBMECs) can help to restore the antiviral state in HIV-infected macrophages, which may be a defense mechanism against HIV neuroinvasion.-
dc.languageeng-
dc.relation.ispartofAntiviral Research-
dc.subjectAntiviral-
dc.subjectBBB-
dc.subjectExosomes-
dc.subjectHBMECs-
dc.subjectTLR3-
dc.titleExosomes contribute to the transmission of anti-HIV activity from TLR3-activated brain microvascular endothelial cells to macrophages-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.antiviral.2016.07.013-
dc.identifier.pmid27496004-
dc.identifier.scopuseid_2-s2.0-84988344405-
dc.identifier.volume134-
dc.identifier.spage167-
dc.identifier.epage171-
dc.identifier.eissn1872-9096-
dc.identifier.isiWOS:000386983800019-

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