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• W1992465083 abstract "extracellular signal-regulated protein kinase E26 transformation-specific-1 human dermal fibroblast interleukin-18 peripheral blood mononuclear cell phytohaemagglutinin A systemic sclerosis TO THE EDITOR Recently, we read with interest the article titled “IL-18 downregulates collagen production in human dermal fibroblasts via the ERK pathway”. In this article, Kim et al., 2010Kim H.J. Song S.B. Choi J.M. et al.IL-18 downregulates collagen production in human dermal fibroblasts via the ERK pathway.J Invest Dermatol. 2010; 130: 706-715Crossref PubMed Scopus (44) Google Scholar reported that IL-18 downregulates collagen production in human dermal fibroblasts directly via the E26 transformation-specific-1 and the ERK pathway, suggesting that IL-18 may exert antifibrotic activities in dermal fibroblasts from patients with systemic sclerosis (SSc). On the basis of these results, the authors concluded that IL-18 may represent a class of modulators with potential usefulness in treating excessive fibrosis in skin. However, an earlier study by Mosaad et al., 2003Mosaad Y.M. Metwally S.S. Auf F.A. et al.Proinflammatory cytokines (IL-12 and IL-18) in immune rheumatic diseases: relation with disease activity and autoantibodies production.Egypt J Immunol. 2003; 10: 19-26PubMed Google Scholar found that serum IL-18 levels in SSc patients were significantly higher than that in a control group, and there was a significant positive correlation between the levels of IL-18 and clinical grades of SSc. Moreover, a study carried out by Scala et al., 2004Scala E. Pallotta S. Frezzolini A. et al.Cytokine and chemokine levels in systemic sclerosis: relationship with cutaneous and internal organ involvement.Clin Exp Immunol. 2004; 138: 540-546Crossref PubMed Scopus (205) Google Scholar found that IL-18 in supernatants from phytohaemagglutinin-stimulated peripheral blood mononuclear cells was increased in SSc patients, and IL-18 production from peripheral blood mononuclear cells was related to kidney involvement. These studies suggest that elevations in the proinflammatory cytokine IL-18 may trigger inflammation in SSc, as IL-18 levels are correlated with disease activity. As described above, studies on the role of IL-18 in SSc seem to be contradictory. In fact, Kim et al., 2010Kim H.J. Song S.B. Choi J.M. et al.IL-18 downregulates collagen production in human dermal fibroblasts via the ERK pathway.J Invest Dermatol. 2010; 130: 706-715Crossref PubMed Scopus (44) Google Scholar discussed in their article that IL-18 has multiple functions and that it participates in both Th1- and Th2-mediated responses. Working in different systems, Zhang et al., 2007Zhang Y. Li P. Li G. et al.The mechanism of how anti-IL-18 prevents concanavalin-A-induced hepatic fibrosis on a mouse model.J Surg Res. 2007; 142: 175-183Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar have reported that hepatic fibrosis is exacerbated by IL-18, which activates CD4+ T cells, and that this effect is blocked by anti-IL-18 treatment Reddy et al., 2008Reddy V.S. Harskamp R.E. van Ginkel M.W. et al.Interleukin-18 stimulates fibronectin expression in primary human cardiac fibroblasts via PI3K-Akt-dependent NF-kappaB activation.J Cell Physiol. 2008; 215: 697-707Crossref PubMed Scopus (55) Google Scholar. Moreover, Reddy et al., 2008Reddy V.S. Harskamp R.E. van Ginkel M.W. et al.Interleukin-18 stimulates fibronectin expression in primary human cardiac fibroblasts via PI3K-Akt-dependent NF-kappaB activation.J Cell Physiol. 2008; 215: 697-707Crossref PubMed Scopus (55) Google Scholar reported that IL-18 upregulates fibronectin expression in primary human cardiac fibroblasts. Therefore, IL-18 may also be regarded as a fibrogenic cytokine. By contrast, there is additional evidence suggesting that IL-18 can also inhibit fibrosis. Nakatani-Okuda et al., 2005Nakatani-Okuda A. Ueda H. Kashiwamura S. et al.Protection against bleomycin-induced lung injury by IL-18 in mice.Am J Physiol Lung Cell Mol Physiol. 2005; 289: L280-L287Crossref PubMed Scopus (37) Google Scholar have reported that IL-18 has a crucial role in protection against bleomycin-induced lung injuries in mice. Zhang et al., 2001Zhang L.H. Pan J.P. Yao H.P. et al.Intrasplenic transplantation of IL-18 gene-modified hepatocytes: an effective approach to reverse hepatic fibrosis in schistosomiasis through induction of dominant Th1 response.Gene Ther. 2001; 8: 1333-1342Crossref PubMed Scopus (26) Google Scholar found that IL-18 reverses hepatic fibrosis and regulates Th1 and Th2 cytokine responses. In summary, IL-18 seems to function both as a profibrotic and antifibrotic mediator of fibrosis, which may depend on the induction of Th1 or Th2 cytokine profiles. We would submit that it is still too early to say that IL-18 can induce SSc or benefit SSc. Additional studies with more patients and animal studies, as well, will be needed to determine the precise roles of IL-18 in SSc. Unraveling the relationship between IL-18 production and the activity of SSc may then allow the identification of relevant targets for therapeutic intervention. This work was partly supported by grants from the key program of National Natural Science Foundation of China (30830089) and the Anhui Provincial Natural Science Foundation (11040606M183)." @default.
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• W1992465083 title "Interleukin-18: Friend or Foe for Systemic Sclerosis?" @default.
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