File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: HIV TAT modulation of IFN-γ-induced expression of autophagy-associated genes in primary human blood macrophages

TitleHIV TAT modulation of IFN-γ-induced expression of autophagy-associated genes in primary human blood macrophages
Authors
Issue Date2009
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine
Citation
The 2009 Tri-Society Annual Conference of the Society for Leukocyte Biology, International Cytokine Society, & International Society for Interferon and Cytokine Research, Cellular and Cytokine Interactions in Health and Disease, Lisbon, Portugal, 17-21 October 2009. In Cytokine, 2009, v. 48 n. 1-2, p. 67 abstract no. PP1-095 How to Cite?
AbstractHuman immunodeficiency virus (HIV), the causative agent of AIDS, continues to be a major cause of morbidity and mortality worldwide. Immune defects in HIV patients are closely associated with intense cytokine dysregulation. HIV trans-activator protein, Tat, plays a critical role in HIV replication; and its induction of apoptosis, Type I programmed cell death, in CD4+ T cells contributes to immune defects. We recently showed that HIV Tat impairs the IFN-γ-receptor signaling pathway at the level of STAT1 phosphorylation due to SOCS-2 activation (Blood 2009). Since IFN-γ was found to induce autophagy, a cellular process proposed to be associated with intracellular killing of M. tuberculosis, we investigated whether HIV Tat can inhibit IFN-γ-induced signaling pathway leading to ultimate downregulation of the IFN-γ-induced autophagy in peripheral blood monocyte derived macrophages (PBMac). We demonstrated that IFN-γ can induce the expression of an autophagy-associated gene, microtubule-associated protein 1 light chain 3 (LC3 I and II) in a time- and dose-dependent manner in human macrophages. With pretreatment of the cells with HIV Tat, the IFN-γ-induced expression of the autophagy-associated gene was suppressed. Tat exerted its activities on IFN-γ-induced effects in a dose-dependent manner. We further showed that HIV Tat inhibition on IFN-γ-induced expression of the autophagy-associated gene was through the suppression of phosphorylated-STAT1 protein generation, by using a specific inhibitor for STAT1 activation. Detailed mechanisms underlying the effects of Tat on the modulation of autophagy-associated genes are in progress. Taken together, modulation of the expression of autophagy-associated genes by HIV Tat may affect mycobacterial survival. These results may have implications in understanding the rampant spread of mycobacterial infection in AIDS.
DescriptionPoster Presentation I
Persistent Identifierhttp://hdl.handle.net/10722/106349
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAu, KYen_HK
dc.contributor.authorLi, JCBen_HK
dc.contributor.authorYim, HCHen_HK
dc.contributor.authorFang, JWen_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-09-25T23:12:02Z-
dc.date.available2010-09-25T23:12:02Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 2009 Tri-Society Annual Conference of the Society for Leukocyte Biology, International Cytokine Society, & International Society for Interferon and Cytokine Research, Cellular and Cytokine Interactions in Health and Disease, Lisbon, Portugal, 17-21 October 2009. In Cytokine, 2009, v. 48 n. 1-2, p. 67 abstract no. PP1-095-
dc.identifier.issn1043-4666-
dc.identifier.urihttp://hdl.handle.net/10722/106349-
dc.descriptionPoster Presentation I-
dc.description.abstractHuman immunodeficiency virus (HIV), the causative agent of AIDS, continues to be a major cause of morbidity and mortality worldwide. Immune defects in HIV patients are closely associated with intense cytokine dysregulation. HIV trans-activator protein, Tat, plays a critical role in HIV replication; and its induction of apoptosis, Type I programmed cell death, in CD4+ T cells contributes to immune defects. We recently showed that HIV Tat impairs the IFN-γ-receptor signaling pathway at the level of STAT1 phosphorylation due to SOCS-2 activation (Blood 2009). Since IFN-γ was found to induce autophagy, a cellular process proposed to be associated with intracellular killing of M. tuberculosis, we investigated whether HIV Tat can inhibit IFN-γ-induced signaling pathway leading to ultimate downregulation of the IFN-γ-induced autophagy in peripheral blood monocyte derived macrophages (PBMac). We demonstrated that IFN-γ can induce the expression of an autophagy-associated gene, microtubule-associated protein 1 light chain 3 (LC3 I and II) in a time- and dose-dependent manner in human macrophages. With pretreatment of the cells with HIV Tat, the IFN-γ-induced expression of the autophagy-associated gene was suppressed. Tat exerted its activities on IFN-γ-induced effects in a dose-dependent manner. We further showed that HIV Tat inhibition on IFN-γ-induced expression of the autophagy-associated gene was through the suppression of phosphorylated-STAT1 protein generation, by using a specific inhibitor for STAT1 activation. Detailed mechanisms underlying the effects of Tat on the modulation of autophagy-associated genes are in progress. Taken together, modulation of the expression of autophagy-associated genes by HIV Tat may affect mycobacterial survival. These results may have implications in understanding the rampant spread of mycobacterial infection in AIDS.-
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine-
dc.relation.ispartofCytokineen_HK
dc.titleHIV TAT modulation of IFN-γ-induced expression of autophagy-associated genes in primary human blood macrophagesen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1043-4666&volume=48&issue=1-2&spage=67 abstract no. PP1&epage=095&date=2009&atitle=HIV+TAT+modulation+of+IFN-γ-induced+expression+of+autophagy-associated+genes+in+primary+human+blood+macrophages-
dc.identifier.emailAu, KY: aukinyi@graduate.hku.hken_HK
dc.identifier.emailLi, JCB: jamesli@graduate.hku.hken_HK
dc.identifier.emailYim, HCH: chhyim@graduate.hku.hken_HK
dc.identifier.emailFang, JW: meifang@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityLi, JCB=rp00496en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.identifier.doi10.1016/j.cyto.2009.07.218-
dc.identifier.hkuros168391en_HK
dc.identifier.volume48-
dc.identifier.issue1-2-
dc.identifier.spage67 abstract no. PP1-095-
dc.identifier.epage67 abstract no. PP1-095-
dc.identifier.isiWOS:000270855100223-
dc.description.otherThe 2009 Tri-Society Annual Conference of the Society for Leukocyte Biology, International Cytokine Society, & International Society for Interferon and Cytokine Research, Cellular and Cytokine Interactions in Health and Disease, Lisbon, Portugal, 17-21 October 2009. In Cytokine, 2009, v. 48 n. 1-2, p. 67 abstract no. PP1-095-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats