Interleukin 18 stimulates HIV type 1 in monocytic cells

Shapiro, Leland; Puren, Adrian; Barton, Hazel A.; Novick, Daniela; Peskind, Robert L.; Shenkar, Robert; Gu, Yun; Su, Michael; Dinarello, Charles A.

doi:10.1073/pnas.95.21.12550

Cited by 103 publications

(90 citation statements)

References 47 publications

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“…Although an early report suggested that IL-18 increased human immunodeficiency virus (HIV)-1 production in a chronically infected monocytic cell line [111], recent studies predict a protective role with IL-18 inhibiting HIV-1 production by peripheral blood cells [112]. In vaccine studies, the coinjection of DNA encoding IL-18 modulates the specific immune response toward a protective Th1 type [113].…”

Section: Viral Infectionsmentioning

confidence: 99%

Interleukin-18

Gracie

Robertson

McInnes

2003

Journal of Leukocyte Biology

638

501

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Abstract:Interleukin-18 (IL-18), a recently described member of the IL-1 cytokine superfamily, is now recognized as an important regulator of innate and acquired immune responses. IL-18 is expressed at sites of chronic inflammation, in autoimmune diseases, in a variety of cancers, and in the context of numerous infectious diseases. This short review will describe the basic biology of IL-18 and thereafter address its potential effector and regulatory role in several human disease states including autoimmunity and infection. IL-18, previously known as interferon-␥ (IFN-␥)-inducing factor, was identified as an endotoxin-induced serum factor that stimulated IFN-␥ production by murine splenocytes

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Section: Viral Infectionsmentioning

confidence: 99%

Interleukin-18

Gracie

Robertson

McInnes

2003

Journal of Leukocyte Biology

638

501

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“…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 Genementioning

confidence: 99%

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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“…Because IL-18 was reported to induce NF B activation (Matsumoto et al, 1997;Shapiro et al, 1998;Torigoe et al, 1997), we investigated whether this transcription factor was involved in the IL-18 -induced IL-8 expression. When NF B is activated, it translocates from the cytoplasm to the nucleus.…”

Section: Il-18 Induces Nuclear Translocation Of Nf B (P65) In Ra Synomentioning

confidence: 99%