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Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation

ABSTRACT: Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation

PROVIDER: PRJNA328275 | ENA |

REPOSITORIES: ENA

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Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation (ChIP-Seq)

Project description:We screened for small molecules that reactivated latent HIV-1 and identified benzotriazoles as latency-reducing agents. Here, we characterize the effects of HODHBt on gene expression in cultured T cells from three donors by polyA RNA-Seq and on STAT5A occupancy of the HIV-1 LTR promoter by ChIP-Seq. These and other results demonstrate that benzotriazoles block SUMOylation of phosphorylated STAT5, prolonging its transcriptional activity.

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Benzotriazoles Reactivate Latent HIV-1 through Inactivation of STAT5 SUMOylation.

Project description: Not available

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Project description:Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation (ChIP-Seq)

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Benzotriazoles reactivate latent HIV-1 through inactivation of STAT5 SUMOylation

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Post-translational modification with SUMO is known to regulate the activity of transcription factors, but how SUMOylation of individual proteins might influence immunity is mostly unexplored. The NFAT transcription factors play an essential role in antigen receptor-mediated gene regulation. SUMOylation of NFATc1 represses IL-2 in vitro, but its role in T cell-mediated immune responses in vivo is not clear. To this end, we generated a novel Nfatc1 transgenic mouse, which prevents SUMO modification of NFATc1. Avoidance of NFATc1 SUMOylation ameliorated experimental autoimmune encephalomyelitis as well as graft-versus-host disease. An elevated IL-2 production promoted Treg expansion and suppressed autoreactive or alloreactive T cells. Mechanistically, increased IL-2 secretion counteracted IL-17 and IFN-γ expression through STAT5 and Blimp-1 induction. Then, Blimp-1 repressed IL-2 itself and the as well induced, proliferation-associated survival factor Bcl2A1. Collectively, we demonstrate that prevention of NFATc1 SUMOylation fine-tunes T-cell responses towards lasting tolerance. Thus, targeting NFATc1 SUMOylation presents a novel and promising strategy to treat T cell-mediated inflammatory diseases.

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