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, Shin Je; Cho, Young Sik; Cho, Min Chul; Shim, Jung‐Hyun; Lee, Kyung Ae; Ko, Kwang Kjune; Choe, Yong Kyung; Park, Sue Nie; Hoshino, Tomoaki; Kim, Soo Hyun; Dinarello, Charles A.; Yoon, Do Young

doi:10.4049/jimmunol.167.1.497

Cited by 111 publications

(76 citation statements)

References 54 publications

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“…According to the strong epidemiologic association between HPV infection and genital SCC, functional studies have defined a role for certain HPV gene variations in the initiation and=or progression of tumor formation. During tumorigenic effects of HPV 16 result at least in part from the ability of the viral oncoproteins E6 and E7 to bind and inactivate the wild-type function of these tumor suppressor gene products [12]. Several types have been identified [14].…”

Section: Introductionmentioning

confidence: 99%

Human Papillomavirus HPV-16 Dna as an Epitheliotropic Virus That Induces Hyperproliferation in Squamous Penile Tissue

Salazar

Mercado

Calzada³

2005

Archives of Andrology

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& The prevalence of human papillomavirus HPV-16DNA sequences in 57 penile carcinoma biopsies was examined using the polymerase chain reaction (PCR) with type specific internal probes, employing HPV consensus primers from the L1 region. The cases comprised 39 typical squamous cell carcinoma and 18 specimens with different subtype. PCR products were analyzed and HPV-16DNA was detected in a high percentage of specimens. Thirty-eight biopsies were HPV-16DNA positive. This determination was correlated with cellular differentiation and growth pattern. Our data corroborates that squamous cell carcinoma was invariably associated with HPV-16DNA.

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Section: Introductionmentioning

confidence: 99%

Human Papillomavirus HPV-16 Dna as an Epitheliotropic Virus That Induces Hyperproliferation in Squamous Penile Tissue

Salazar

Mercado

Calzada³

2005

Archives of Andrology

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“…This indicates that an active microbial infection is not absolutely necessary to initiate IL-12 and IL-18 synthesis, and that inert microbial components may be the minimal requirement for the production of these inflammatory factors. The importance of these cytokines in antiviral host defense may also be extrapolated from the knowledge that certain herpesviruses selectively reduce IL-12 production (14), and both poxviruses and papillomaviruses express IL-18-binding proteins that greatly suppress IL-18 activity (15,16).…”

mentioning

confidence: 99%

Activation of Virus-Specific CD8+ T Cells by Lipopolysaccharide-Induced IL-12 and IL-18

Raué

Brien

Hammarlund

et al. 2004

The Journal of Immunology

105

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Virus-specific T cells represent a hallmark of Ag-specific, adaptive immunity. However, some T cells also demonstrate innate functions, including non-Ag-specific IFN-γ production in response to microbial products such as LPS or exposure to IL-12 and/or IL-18. In these studies we examined LPS-induced cytokine responses of CD8+ T cells directly ex vivo. Following acute viral infection, 70–80% of virus-specific T cells will produce IFN-γ after exposure to LPS-induced cytokines, and neutralization experiments indicate that this is mediated almost entirely through production of IL-12 and IL-18. Different combinations of these cytokines revealed that IL-12 decreases the threshold of T cell activation by IL-18, presenting a new perspective on IL-12/IL-18 synergy. Moreover, memory T cells demonstrate high IL-18R expression and respond effectively to the combination of IL-12 and IL-18, but cannot respond to IL-18 alone, even at high cytokine concentrations. This demonstrates that the synergy between IL-12 and IL-18 in triggering IFN-γ production by memory T cells is not simply due to up-regulation of the surface receptor for IL-18, as shown previously with naive T cells. Together, these studies indicate how virus-specific T cells are able to bridge the gap between innate and adaptive immunity during unrelated microbial infections, while attempting to protect the host from cytokine-induced immunopathology and endotoxic shock.

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“…Similarly, E7 also inhibits the expression of α-IFNresponsive genes [56,57]. Also these two oncoproteins can reduce expression of Toll-like receptor (TLR) 9 [58], and some cytokines, such as IL-8 and IL-18 [59,60]. TLR 9 is expressed in endosomal vesicles where it binds to unmethylated CpG sequences in viral DNA.…”

Section: Mechanisms Of Hpv To Evade the Immune Systemmentioning

confidence: 99%

Prophylactic and Therapeutic Vaccines against Human Papillomavirus Infections

Rosales¹,

Rosales²

2017

Vaccines

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Human papillomaviruses (HPVs) are a large family of double-strand DNA viruses comprising more than 180 types. Infection with HPV is associated with benign and malignant proliferation of skin and mucosae. Low-risk HPVs produce warts, whereas high-risk viruses induce tumors. Because there are no anti-viral drugs for HPV infection, there is a lot of interest in vaccines that can prevent the infection and also in vaccines that can be used to treat established infections and HPV-related tumors. Two prophylactic vaccines have been approved for preventing HPV infection. They seem to be efective when very young people are vaccinated. Unfortunately, many older people are still at risk of infection, mainly in countries where vaccination coverage is not eicient and for those people, novel therapeutic vaccines are being developed. This chapter describes the properties of HPV vaccines used today and the current status of several therapeutic vaccines been developed to treat HPV-induced lesions.

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

Cited by 111 publications

References 54 publications

Human Papillomavirus HPV-16 Dna as an Epitheliotropic Virus That Induces Hyperproliferation in Squamous Penile Tissue

Human Papillomavirus HPV-16 Dna as an Epitheliotropic Virus That Induces Hyperproliferation in Squamous Penile Tissue

Activation of Virus-Specific CD8+ T Cells by Lipopolysaccharide-Induced IL-12 and IL-18

Prophylactic and Therapeutic Vaccines against Human Papillomavirus Infections

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