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Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

ABSTRACT: IL-27 treated DCs were shown to be highly potent inhibitors of cis HIV-1, particularly of CCR5 tropic strains. Microarray studies of IL-27 treated DCs showed no up-regulation of Type I (IFN) gene expression. Neutralization of the Type-I IFN receptor had no impact on the HIV inhibition. Lastly, IL-27 mediated inhibition was shown to act post-viral entry and prior to completion of reverse transcription. These results show for the first time that IL-27 is a potent inhibitor of cis HIV-1 infection in DCs by a Type I IFN independent mechanism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44732 | GEO | 2013/03/29

SECONDARY ACCESSION(S): PRJNA191106

REPOSITORIES: GEO

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Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

Project description:IL-27 treated DCs were shown to be highly potent inhibitors of cis HIV-1, particularly of CCR5 tropic strains. Microarray studies of IL-27 treated DCs showed no up-regulation of Type I (IFN) gene expression. Neutralization of the Type-I IFN receptor had no impact on the HIV inhibition. Lastly, IL-27 mediated inhibition was shown to act post-viral entry and prior to completion of reverse transcription. These results show for the first time that IL-27 is a potent inhibitor of cis HIV-1 infection in DCs by a Type I IFN independent mechanism. Gene expression microarrays from 3 samples of immature dendritic cells (iDCs) were compared with 3 samples of iDCs treated with IL-27

2013-03-29 | E-GEOD-44732 | biostudies-arrayexpress

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Project description:HIV-specific T cells have diminished effector function and fail to control/eliminate the virus. IL-27, a member of the IL-6/IL-12 cytokine superfamily has been shown to inhibit HIV replication however whether IL-27 can enhance function on HIV-specific T cell is largely unknown. Because of the important implication in cure strategies, in the present manuscript, we investigated the role of IL-27 signaling in human T cells by evaluating the global transcriptional changes and its impact in the function of HIV-specific T cells. We found that T cells from people living with HIV (PLWH), expressed higher levels of STAT1 that leads to enhanced STAT1 activation upon IL-27 stimulation. IL-27 induced transcriptional changes associated with IFN/STAT1-dependent pathways in CD4 and CD8 T cells. More importantly, IL-27 promoted cytokine secretion of TIGIT+HIVGag-specific T cell function by modulating the expression levels of T-bet. This new immunomodulatory property of IL-27 on HIV-specific T cell function suggests its potential therapeutic use in cure strategies.

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Project description:Type I interferons (IFNs) exert a broad range of biological effects important in coordinating immune responses, which have classically been studied in the context of pathogen clearance. Yet, whether immunomodulatory bacteria operate through IFN pathways to support intestinal immune tolerance remains elusive. Here, we reveal that the commensal bacterium, Bacteroides fragilis, utilizes canonical antiviral pathways to modulate intestinal dendritic cells (DCs) and regulatory T cell (Treg) responses. Specifically, IFN signaling is required for commensal-induced tolerance, as IFNAR1-deficient DCs display blunted IL-10 and IL-27 production in response to B. fragilis. We further establish that IFN-driven IL-27 in DCs is critical in shaping the ensuing Foxp3+ Treg via IL27Ra signaling. Consistent with these findings, single cell RNA sequencing of gut Tregs demonstrated that colonization with B. fragilis promotes a distinct IFN gene signature in Foxp3+ Tregs during intestinal inflammation. Altogether, our findings demonstrate a critical role of commensal-mediated immune tolerance via tonic type I IFN signaling.

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IL-27 Inhibits HIV-1 Infection in Human Macrophages by Down-regulating Host Factor SPTBN1 during Monocyte to Macrophage Differentiation

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