Interleukin-18 in Health and Disease | ||||
| Suez Canal University Medical Journal | ||||
| Editorial, Volume 16, Issue 2, October 2013, Page 78-86 PDF (264.85 K) | ||||
| DOI: 10.21608/scumj.2013.54218 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Howayda M Hassoba   ; Rania M Saleh
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| Department of Clinical Pathology, Faculty of Medicine, Suez Canal University | ||||
| Abstract | ||||
| Interleukin-18 (IL-18) is a relatively newly discovered immunostimulatory cytokine, which is structurally similar to IL-1. IL-18 is produced mainly by activated macrophages, however; it may also be expressed by kupffer cells, T cells, B cells, keratinocytes, astrocytes, and osteoblasts. IL-18 can regulate both innate and adaptive immune responses through its effects on natural killer (NK) cells, monocytes, dendritic cells, T cells, and B cells. IL-18 has multiple biological activities via its capacity to stimulate innate immunity and both Th1 and Th2 mediated responses. IL-18 acts synergistically with other pro-inflammatory cytokines to promote interferon-γ (IFN-γ) production by NK cells, T cells, and possibly other cell types. It induces gene expression and synthesis of Tumor Necrosis Factor (TNF), IL-1, Fas Ligand, and several chemokines. It also exerts anti-tumor effects that are mediated by enhancement of Natural Killer (NK) cell activity, reduction of tumorigenesis, induction of apoptosis and inhibition of angiogenesis in tumor cells. IL-18 plays a critical role in the Th1 response required for host defense against viruses as well as plays a role in inflammatory liver disease. IL-18 was significantly upregulated in persons with chronic HCV infection compared to healthy persons or asymptomatic carriers. This upregulation correlated with hepatic injury, indicating a role for IL-18 in the pathogenesis of HCV infection. In addition, neutralization of IL-18 by administration of anti-IL-18 monoclonal antibodies (mAb) results in total prevention of liver injury. Raised levels of serum IL-18 was demonstrated in chronic HCV-patients before antiviral therapy with Pegylated IFN (PEG-IFN). A marked decline in IL-18 was associated with remission of hepatic inflammatory activity in responders, while persistent raised levels of IL-18 were associated with PEG-IFN treatment failure. | ||||
| Keywords | ||||
| HCV; Cytokines; Interleukins | ||||
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