IFN-γ-induced BST2 mediates monocyte adhesion to human endothelial cells

Yoo, Hyouna; Park, Sang Ho; Ye, Sang Kyu; Kim, Myung

doi:10.1016/j.cellimm.2010.10.011

Cited by 50 publications

(54 citation statements)

References 23 publications

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“…It is well known that BST-2 expression is principally induced by IFNs (Jones et al, 2013; Jones et al, 2012a; Yoo et al, 2011). To assess the level of types I and II IFN during MMTV pathogenesis and to determine whether levels of IFNs correlate with BST-2, we evaluated the transcripts of IFNα and IFNγ in representative lymphoid, mammary, and tumor tissues from naïve, infected, and tumor-bearing mice.…”

Section: Resultsmentioning

confidence: 99%

BST-2/tetherin is overexpressed in mammary gland and tumor tissues in MMTV-induced mammary cancer

et al. 2013

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BST-2 restricts MMTV replication, but once infection has established, MMTV modulates BST-2 levels. MMTV-directed BST-2 modulation is tissue-specific and dependent on infection and neoplastic transformation status of cells. In the lymphoid compartment of infected mice, BST-2 expression is first upregulated and then significantly downregulated regardless of absence or presence of mammary tumors. However, in mammary gland tissues, upregulation of BST-2 expression is dependent on the presence of mammary tumors and tumor tissues themselves have high BST-2 levels. Elevated BST-2 expression in these tissues is not attributable to IFN since levels of IFNα and IFNγ negatively correlate with BST-2. Importantly, soluble factors released by tumor cells suppress IFNα and IFNγ but induce BST-2. These data suggest that overexpression of BST-2 in carcinoma tissues could not be attributed to IFNs but to a yet to be determined factor that upregulates BST-2 once oncogenesis is initiated.

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Section: Resultsmentioning

confidence: 99%

BST-2/tetherin is overexpressed in mammary gland and tumor tissues in MMTV-induced mammary cancer

et al. 2013

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“…It is possible that BST‐2 uses this mechanism to “tether” cells to each other thereby promoting cell‐to‐cell interaction. Indeed, BST‐2 mediates adhesion of monocytes to endothelial cells 132. The ability of BST‐2 to mediate adhesion was also demonstrated in breast cancer cells where suppression of BST‐2 significantly decreased cell‐to‐cell interaction as well as cell to extracellular matrix (ECM) interactions with collagen and fibronectin 122 (Fig.…”

Section: Bst‐2/tetherin: Roles In Carcinogenesismentioning

confidence: 87%

The role of BST‐2/Tetherin in host protection and disease manifestation

Mahauad‐Fernandez

Okeoma

2015

Immunity, Inflammation and Disease

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Host cells respond to viral infections by activating immune response genes that are not only involved in inflammation, but may also predispose cells to cancerous transformation. One such gene is BST‐2, a type II transmembrane protein with a unique topology that endows it tethering and signaling potential. Through this ability to tether and signal, BST‐2 regulates host response to viral infection either by inhibiting release of nascent viral particles or in some models inhibiting viral dissemination. However, despite its antiviral functions, BST‐2 is involved in disease manifestation, a function linked to the ability of BST‐2 to promote cell‐to‐cell interaction. Therefore, modulating BST‐2 expression and/or activity has the potential to influence course of disease.

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“…Many studies have suggested that BST-2 expression could be induced by type I IFN (5,6,14,25,36,48) and type II IFN (6,14,68,71) in different cell types of human and mouse origin. Consistent with these findings, analysis of the putative promoter region of human, nonhuman primate, and mouse BST2 identified several highly conserved TFBS that would support this type of regulation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Virus-Activated Interferon Regulatory Factor 7 Upregulates Expression of the Interferon-Regulated BST2 Gene Independently of Interferon Signaling

Bego

Mercier

Cohen

2012

J Virol

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bBST-2/tetherin is an interferon (IFN)-inducible host restriction factor that inhibits the release of many enveloped viruses and functions as a negative-feedback regulator of IFN production by plasmacytoid dendritic cells. Currently, mechanisms underlying BST2 transcriptional regulation by type I IFN remain largely unknown. Here, we demonstrate that the BST2 promoter is a secondary target of the IFN cascade and show that a single IRF binding site is sufficient to render this promoter responsive to IFN-␣. Interestingly, expression of IRF-1 or virus-activated forms of IRF-3 and IRF-7 stimulated the BST2 promoter even under conditions where type I IFN signaling was inhibited. Indeed, vesicular stomatitis virus could directly upregulate BST-2 during infection of mouse embryonic fibroblasts through a process that required IRF-7 but was independent from the type I IFN cascade; however, in order to achieve optimal BST-2 induction, the type I IFN cascade needed to be engaged through activation of IRF-3. Furthermore, using human peripheral blood mononuclear cells, we show that BST-2 upregulation is part of an early intrinsic immune response since TLR8 and TLR3 agonists, known to trigger pathways that mediate activation of IRF proteins, could upregulate BST-2 prior to engagement of the type I IFN pathway. Collectively, our findings reveal that BST2 is activated by the same signals that trigger type I IFN production, outlining a regulatory mechanism ensuring that production of type I IFN and expression of a host restriction factor involved in the IFN negative-feedback loop are closely coordinated.

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IFN-γ-induced BST2 mediates monocyte adhesion to human endothelial cells

Cited by 50 publications

References 23 publications

BST-2/tetherin is overexpressed in mammary gland and tumor tissues in MMTV-induced mammary cancer

BST-2/tetherin is overexpressed in mammary gland and tumor tissues in MMTV-induced mammary cancer

The role of BST‐2/Tetherin in host protection and disease manifestation

Virus-Activated Interferon Regulatory Factor 7 Upregulates Expression of the Interferon-Regulated BST2 Gene Independently of Interferon Signaling

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