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Article: Human cervical epithelial cells release antiviral factors and inhibit HIV replication in macrophages

TitleHuman cervical epithelial cells release antiviral factors and inhibit HIV replication in macrophages
Authors
KeywordsHIV
Human cervical epithelial cells
Interferon-stimulated genes
Macrophages
Toll-like receptor 3
Issue Date2018
Citation
Journal of Innate Immunity, 2018, v. 11, n. 1, p. 29-40 How to Cite?
AbstractThe female reproductive tract is a major site of HIV sexual transmission. We here examined whether human cervical epithelial cells (HCEs) can be immunologically activated and produce antiviral factors against HIV. We demonstrated that HCEs (End1/E6E7 cells) possess the functional toll-like receptor (TLR)3 signaling system, which could be activated by Poly I:C and induce multiple cellular HIV restriction factors. The treatment of primary human macrophages with supernatant (SN) from TLR3-activated End1/E6E7 cell cultures resulted in HIV inhibition. This SN-mediated HIV inhibition was mainly through the induction of interferons (IFN)-β and IFN-λs, as the antibodies to IFN-β or IFN-λs receptor could effectively block the SN-mediated anti-HIV effect. Further studies showed that the incubation of macrophages with SN from the activated cervical epithelial cell cultures induced the expression of a number of IFN-stimulated genes (ISGs), including IFN-stimulated gene (ISG15), ISG56, 2′, 5′-oligoadenylate synthetase 1 (OAS 1), OAS 2, Myxovirus Resistance A (MxA), MxB, and Guanylate-binding protein 5 (GBP5). In addition, TLR3-activated cells produced the CC chemokines [regulated on activation, normal T cell expressed and secreted (RANTES), Human macrophage inflammatory protein 1 alpha (MIP-1α), MIP-1β] the ligands of HIV entry co-receptor CCR5. These observations support further studies on HCEs as potentially crucial and alternative targets for immunological intervention to control and prevent HIV sexual transmission.
Persistent Identifierhttp://hdl.handle.net/10722/322049
ISSN
2021 Impact Factor: 7.111
2020 SCImago Journal Rankings: 2.078
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXu, Xi Qiu-
dc.contributor.authorGuo, Le-
dc.contributor.authorWang, Xu-
dc.contributor.authorLiu, Yu-
dc.contributor.authorLiu, Hang-
dc.contributor.authorZhou, Run Hong-
dc.contributor.authorGu, Jun-
dc.contributor.authorLiu, Jin Biao-
dc.contributor.authorXu, Pei-
dc.contributor.authorZhou, Li-
dc.contributor.authorHo, Wen Zhe-
dc.date.accessioned2022-11-03T02:23:15Z-
dc.date.available2022-11-03T02:23:15Z-
dc.date.issued2018-
dc.identifier.citationJournal of Innate Immunity, 2018, v. 11, n. 1, p. 29-40-
dc.identifier.issn1662-811X-
dc.identifier.urihttp://hdl.handle.net/10722/322049-
dc.description.abstractThe female reproductive tract is a major site of HIV sexual transmission. We here examined whether human cervical epithelial cells (HCEs) can be immunologically activated and produce antiviral factors against HIV. We demonstrated that HCEs (End1/E6E7 cells) possess the functional toll-like receptor (TLR)3 signaling system, which could be activated by Poly I:C and induce multiple cellular HIV restriction factors. The treatment of primary human macrophages with supernatant (SN) from TLR3-activated End1/E6E7 cell cultures resulted in HIV inhibition. This SN-mediated HIV inhibition was mainly through the induction of interferons (IFN)-β and IFN-λs, as the antibodies to IFN-β or IFN-λs receptor could effectively block the SN-mediated anti-HIV effect. Further studies showed that the incubation of macrophages with SN from the activated cervical epithelial cell cultures induced the expression of a number of IFN-stimulated genes (ISGs), including IFN-stimulated gene (ISG15), ISG56, 2′, 5′-oligoadenylate synthetase 1 (OAS 1), OAS 2, Myxovirus Resistance A (MxA), MxB, and Guanylate-binding protein 5 (GBP5). In addition, TLR3-activated cells produced the CC chemokines [regulated on activation, normal T cell expressed and secreted (RANTES), Human macrophage inflammatory protein 1 alpha (MIP-1α), MIP-1β] the ligands of HIV entry co-receptor CCR5. These observations support further studies on HCEs as potentially crucial and alternative targets for immunological intervention to control and prevent HIV sexual transmission.-
dc.languageeng-
dc.relation.ispartofJournal of Innate Immunity-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectHIV-
dc.subjectHuman cervical epithelial cells-
dc.subjectInterferon-stimulated genes-
dc.subjectMacrophages-
dc.subjectToll-like receptor 3-
dc.titleHuman cervical epithelial cells release antiviral factors and inhibit HIV replication in macrophages-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1159/000490586-
dc.identifier.pmid30032138-
dc.identifier.pmcidPMC6338329-
dc.identifier.scopuseid_2-s2.0-85058762244-
dc.identifier.volume11-
dc.identifier.issue1-
dc.identifier.spage29-
dc.identifier.epage40-
dc.identifier.eissn1662-8128-
dc.identifier.isiWOS:000455065600004-

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