Repression of the interferon signal transduction pathway by the adenovirus E1A oncogene.

Gutch, Michael J.; Reich, Nancy C.

doi:10.1073/pnas.88.18.7913

Cited by 97 publications

(75 citation statements)

References 40 publications

(68 reference statements)

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“…CIITA is recruited to the MHC promoter via specific protein-protein interactions with the MHC activators (37). Similar to effects described in other IFN-responsive systems (14,18), the E1A protein, as we show here, can suppress IFN-␥-induced transcription of the E␣ MHC class II promoter. In addition, E1A strongly inhibits the activity of the same promoter in B lymphoid cells.…”

Section: Discussionsupporting

confidence: 89%

“…In macrophages, glucocorticoids, prostaglandins, and IFN-␣/␤ antagonize the action of IFN-␥, which together with interleukin 4 is the main positive regulator of MHC class II genes (11,13). The adenoviral oncoprotein E1A has a strong inhibitory effect on IFN-inducible gene activity in many systems, including the MHC class II genes (14,18). E1A oncoprotein is a pleiotropic molecule able to modulate the expression of various cellular genes (3).…”

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confidence: 99%

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Involvement of CREB Binding Protein in Expression of Major Histocompatibility Complex Class II Genes via Interaction with the Class II Transactivator

Kretsovali

Agalioti

Spilianakis

et al. 1998

Molecular and Cellular Biology

159

138

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The class II transactivator (CIITA) is a key regulatory factor that controls expression of the major histocompatibility complex (MHC) class II genes that are essential components for antigen presentation and thus regulation of the immune response. We show here that the adenovirus E1A protein interferes with the action of CIITA and inhibits both B-cell-specific and gamma interferon (IFN-γ)-induced expression of MHC class II promoters. Transfection studies provide evidence for the functional role of the CREB-binding protein (CBP) in IFN-γ and CIITA-mediated MHC class II promoter activation. We demonstrate that the N-terminally located transcription activation domain of CIITA physically interacts with both the N-terminal and the E1A-binding (C/H3) regions of CBP. These results suggest the involvement of a multisubunit complex, which contains the gene-specific coactivator CIITA and the versatile coactivator CBP, in MHC class II gene regulation, which may be responsible for both high-level expression and modulation by different signaling pathways.

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Involvement of CREB Binding Protein in Expression of Major Histocompatibility Complex Class II Genes via Interaction with the Class II Transactivator

Kretsovali

Agalioti

Spilianakis

et al. 1998

Molecular and Cellular Biology

159

138

View full text Add to dashboard Cite

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“…However, this is not so surprising, although HPV is equipped with counteracting tools against important host factors, such as IL-18 or IFNs. Many DNA viruses, rather then RNA viruses, have strategies to resist IFNs (58,59). The viral response against IL-18 has recently been shown, especially in human poxviruses.…”

Section: Discussionmentioning

confidence: 99%

Both E6 and E7 Oncoproteins of Human Papillomavirus 16 Inhibit IL-18-Induced IFN-γ Production in Human Peripheral Blood Mononuclear and NK Cells

Lee

Cho

et al. 2001

The Journal of Immunology

107

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Cervical carcinoma is the predominant cancer among malignancies in women throughout the world, and human papillomavirus (HPV) 16 is the most common agent linked to human cervical carcinoma. The present study was performed to investigate the mechanisms of immune escape in HPV-induced cervical cancer cells. The presence of HPV oncoproteins E6 and E7 in the extracellular fluids of HPV-containing cervical cancer cell lines SiHa and CaSki was demonstrated by ELISA. The effect of HPV 16 oncoproteins E6 and E7 on the production of IFN-γ by IL-18 was assessed. E6 and E7 proteins reduced IL-18-induced IFN-γ production in both primary PBMCs and the NK0 cell line. FACS analysis revealed that the viral oncoproteins reduced the binding of IL-18 to its cellular surface receptors on NK0 cells, whereas there was no effect of oncoproteins on IL-1 binding to its surface IL-1 receptors on D10S, a subclone of the murine Th cell D10.G4.1. In vitro pull-down assays also revealed that the viral oncoproteins and IL-18 bound to IL-18R α-chain competitively. These results suggest that the extracellular HPV 16 E6 and E7 proteins may inhibit IL-18-induced IFN-γ production locally in HPV lesions through inhibition of IL-18 binding to its α-chain receptor. Down-modulation of IL-18-induced immune responses by HPV oncoproteins may contribute to viral pathogenesis or carcinogenesis.

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“…EMSA was performed as described (19) with double-stranded oligonucleotide probe representing the GAS site from the interferon regulatory factor-1 (IRF-1) gene 5Ј-GCCTGATTTCCCCGAAATGACGG-3Ј (Ϫ129 to Ϫ107) (26) or the IL-4 receptor gene 5Ј-AGCTTCTTCATCTGAAAAGGG-3Ј (Ϫ407 to Ϫ387) (27). Anti-STAT6 antibody (S-20, Santa Cruz Biotechnology, Santa Cruz, CA), anti-STAT1 antibody (28), anti-influenza hemagglutinin epitope antibody (HA) (12CA5, Boehringer Mannheim), control rabbit polyclonal serum, or control murine monoclonal antibody (gift of J .P. Quigley, SUNY, Stony Brook, NY) were incubated with nuclear extract 20 min prior to addition of probe.…”

Section: Methodsmentioning

confidence: 99%

Interleukin-4-induced STAT6 Recognizes and Activates a Target Site in the Promoter of the Interleukin-4 Receptor Gene

Kotanides

Reich

1996

Journal of Biological Chemistry

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Cytokines function as protein mediators that play a critical role in host defense and serve as a communication link between cells of native and acquired immunity. Cells respond to cytokines with specific biological changes that are dependent on the activation of new gene expression. Studies of the mechanism by which signals are mediated from the receptor to the nucleus by the interferon cytokines have revealed the activation by tyrosine phosphorylation of latent cytoplasmic transcription factors that subsequently translocate to the nucleus (1-4). This pathway has served as a model for signal transmission by many other cytokines including interleukin-4 (IL-4).

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Repression of the interferon signal transduction pathway by the adenovirus E1A oncogene.

Abstract: The

Cited by 97 publications

References 40 publications

Involvement of CREB Binding Protein in Expression of Major Histocompatibility Complex Class II Genes via Interaction with the Class II Transactivator

Involvement of CREB Binding Protein in Expression of Major Histocompatibility Complex Class II Genes via Interaction with the Class II Transactivator

Both E6 and E7 Oncoproteins of Human Papillomavirus 16 Inhibit IL-18-Induced IFN-γ Production in Human Peripheral Blood Mononuclear and NK Cells

Interleukin-4-induced STAT6 Recognizes and Activates a Target Site in the Promoter of the Interleukin-4 Receptor Gene

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