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IL-27 increases BST-2 expression in human monocytes and T cells independently of type I IFN.

ABSTRACT: IL-27 modulates inflammatory responses by influencing cytokine secretion and CD4 T cell differentiation. Recently, IL-27 was demonstrated to inhibit HIV replication by inducing type I interferon (IFN) expression and subsequent IFN-dependent expression of apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC)-3 family members, a group of antiviral cytidine deaminases. To characterize other anti-viral genes modulated by IL-27, we examined another IFN-responsive gene: tetherin/bone marrow stromal cell antigen 2 (BST-2). Our study shows that IL-27 can directly induce BST-2 expression, independently of an intermediary type I IFN response. Quantitative RT-PCR analysis demonstrated IL-27-induced BST-2 mRNA expression as early as 2h after exposure of cells to IL-27. In the presence of the type I IFN-neutralizing protein, B18R, IL-27-induced BST-2 expression was maintained, demonstrating that IFN is not an intermediary in IL-27-induced BST-2. Taken together, our findings identify a novel function of IL-27 as a direct stimulator of BST-2 expression.

SUBMITTER: Guzzo C

PROVIDER: S-EPMC3521153 | biostudies-other | 2012

REPOSITORIES: biostudies-other

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Type I IFN augments IL-27-dependent TRIM25 expression to inhibit HBV replication.

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IL-27 induces IFN/STAT1-dependent genes and enhances function of TIGIT<sup>+</sup> HIVGag-specific T cells.

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