In Vivo Antiviral Effect of Interleukin 18 in a Mouse Model of Vaccinia Virus Infection

Tanaka-Kataoka, Mari; Kunikata, Toshio; Takayama, Shojiro; Iwaki, Kanso; Ohashi, Kunihiro; Ikeda, Masao; Kurimoto, Masashi

doi:10.1006/cyto.1998.0453

Cited by 90 publications

(63 citation statements)

References 16 publications

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“…However, the inhibitory effect on the replication of hepatitis B virus indicated a protective role for IL-18 during viral infections, which was explained by IFN-γ production by hepatic NK cells and NK T cells stimulated by IL-18 22 . Similar effects were observed in other viral mouse models 23,24 . Interestingly, in a monocytic cell line, IL-18 stimulated HIV replication 25 .…”

Section: Relationships Between Treatment Response and The Il-18 Gene supporting

confidence: 86%

Impact of the IL-18 gene polymorphism in response to antiviral therapy in chronic HCV genotype 4 patients

Mandour

Nemr

Kishk

et al. 2014

Rev. Soc. Bras. Med. Trop.

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Introduction: Interleukin (IL)-18 is a well-known major proinfl ammatory cytokine with broad biological effects. The major immunomodulatory functions of IL-18 include enhancing T cell and natural killer cell cytotoxicity. Serum levels of this cytokine were shown to increase in chronic hepatitis C patients compared to non-infected healthy people. An association between IL-18 gene promoter polymorphisms and pegylated interferon (PEG-IFN) and ribavirin treatment outcomes has been reported for individuals with chronic hepatitis C virus genotype 1 (HCV-1). In this study, HCV genotype 4 (HCV-4) patients were assessed for IL-18 gene polymorphisms and treatment outcomes or severity of liver disease because data concerning the impact of IL-18 gene polymorphisms on patients with HCV-4 infections are limited. Methods: This study included 123 chronic HCV-4 Egyptian patients and 123 apparently healthy volunteer blood donors who served as a control group. HCV genotyping was performed using the line probe assay. IL-18 genotyping was performed using the TaqMan Real-Time PCR method in all 246 patient and control samples. Results: In our study, all patients had HCV-4. IL-18 gene single nucleotide polymorphism (SNP) (-607C/A) genotype distributions and allele frequencies did not differ between HCV patients and normal healthy subjects or between patient groups when compared according to the therapeutic response. Moreover, the presence of an IL-18 SNP was not associated with histological disease severity. We conclude that the presence of the IL-18 SNP rs1946518 does not affect the outcome of chronic HCV-4 treatment in Egyptian patients. Conclusions: The IL-18 SNP rs1946518 does not affect response to treatment in chronic HCV-4 patients.

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Section: Relationships Between Treatment Response and The Il-18 Gene supporting

confidence: 86%

Impact of the IL-18 gene polymorphism in response to antiviral therapy in chronic HCV genotype 4 patients

Mandour

Nemr

Kishk

et al. 2014

Rev. Soc. Bras. Med. Trop.

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“…DCs and fibroblasts transfected with IL-18 become effective tumor vaccines (36,38). Even injection of rIL-18 alone can combat fungal (56), bacterial (31,32), and viral infections (34,57). Importantly, in all of these studies, IL-18 enhanced Th1 or CTL responses in vivo.…”

Section: Discussionmentioning

confidence: 99%

IL-18 Bridges Innate and Adaptive Immunity through IFN-γ and the CD134 Pathway

Maxwell

Yadav

Rossi

et al. 2006

The Journal of Immunology

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IL-18 induces inflammation resulting in either enhanced protection from pathogens or exacerbation of autoimmunity, and T cells are profoundly activated during these responses. How IL-18 influences T cell activation is unknown, but this study in mice shows that IL-18 boosted Ag-specific T cell clonal expansion of effector T cells and induced a subpopulation of IFN-γ superproducing T cells. Commitment to IFN-γ production through IL-18 was independent of NK cells and IL-12 but dependent on host-derived IFN-γ. To determine how expansion of these effectors occurred, IL-18 was shown to induce OX40L on dendritic cells, whereas peptide stimulation induced CD134 (OX40) on specific T cells. CD134 blockade inhibited T cell effector expansion thereby reducing the number of IFN-γ superproducers by 12-fold. Thus, independent of IL-12, IL-18 impacts T cell immunity throughout lymphoid and nonlymphoid tissue by bridging the innate and adaptive arms of the immune system through IFN-γ and the CD134 costimulatory pathway.

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“…For example, IL-18 was reported to play a major role in resistance against Yersinia, mycobacterial, cryptococcal, Salmonella, Leishmania, herpes simplex virus type 1, feline leukemia virus, and vaccinia virus infections (51)(52)(53)(54)(55)(56)(57)(58). Similar to H. pylori, these infectious agents elicit Th1-dominated immune responses (51,52,55,57,59).…”

Section: Discussionmentioning

confidence: 99%

Vaccine-Induced Immunity againstHelicobacter pyloriInfection Is Impaired in IL-18-Deficient Mice

Akhiani

Schön

Lycke

2004

The Journal of Immunology

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Protective immunity against Helicobacter pylori infection in mice has been associated with a strong Th1 response, involving IL-12 as well as IFN-γ, but recent studies have also demonstrated prominent eosinophilic infiltration, possibly linked to local Th2 activity in the gastric mucosa. In this study we investigated the role of IL-18, because this cytokine has been found to be a coregulator of Th1 development as well as involved in Th2-type responses with local eotaxin production that could influence gastric eosinophilia and resistance to infection. We found that IL-18−/− mice failed to develop protection after oral immunization with H. pylori lysate and cholera toxin adjuvant, indicating an important role of IL-18 in protection. Well-protected C57BL/6 wild-type (WT) mice demonstrated substantial influx of CD4+ T cells and eosinophilic cells in the gastric mucosa, whereas IL-18−/− mice had less gastritis, few CD4+ T cells, and significantly reduced numbers of eosinophilic cells. T cells in well-protected WT mice produced increased levels of IFN-γ and IL-18 to recall Ag. By contrast, unprotected IL-18−/− mice exhibited significantly reduced gastric IFN-γ and specific IgG2a Ab levels. Despite differences in gastric eosinophilic cell infiltration, protected WT and unprotected IL-18−/− mice had comparable levels of local eotaxin, suggesting that IL-18 influences protection via Th1 development and IFN-γ production rather than through promoting local production of eotaxin and eosinophilic cell infiltration.

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In Vivo Antiviral Effect of Interleukin 18 in a Mouse Model of Vaccinia Virus Infection

Cited by 90 publications

References 16 publications

Impact of the IL-18 gene polymorphism in response to antiviral therapy in chronic HCV genotype 4 patients

Impact of the IL-18 gene polymorphism in response to antiviral therapy in chronic HCV genotype 4 patients

IL-18 Bridges Innate and Adaptive Immunity through IFN-γ and the CD134 Pathway

Vaccine-Induced Immunity againstHelicobacter pyloriInfection Is Impaired in IL-18-Deficient Mice

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