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Volume 2013 (2013), Article ID 850851, 6 pages
Stronger Correlation between Interleukin 18 and Soluble Fas in Lupus Nephritis Compared with Mild Lupus
1Rheumatology, Rheumatic Diseases Research Center (RDRC), School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2Rheumatology, Rheumatology Department, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
3Immunology, Immunology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Received 16 January 2013; Accepted 13 February 2013
Academic Editors: A. M. Huber, A. Spreafico, and A. Wong
Copyright © 2013 Mohammad Reza Hatef et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- R. Saxena, T. Mahajan, and C. Mohan, “Lupus nephritis: current update,” Arthritis Research & Therapy, no. 13, article 240, 2011.
- F. A. Houssiau, C. Vasconcelos, D. D'Cruz et al., “Immunosuppressive therapy in lupus nephritis: the Euro-Lupus Nephritis Trial, a randomized trial of low-dose versus high-dose intravenous cyclophosphamide,” Arthritis & Rheumatism, vol. 46, no. 8, pp. 2121–2131, 2002.
- M. Alecu, G. Coman, and S. Alecu, “Serological levels of apoptotic bodies, sFAS and TNF in lupus erythematosus,” Romanian Journal of Internal Medicine, vol. 38, pp. 83–88, 2000.
- A. Gigante, M. L. Gasperini, A. Afeltra et al., “Cytokines expression in SLE nephritis,” European Review for Medical and Pharmacological Sciences, vol. 15, no. 1, pp. 15–24, 2011.
- J. M. Kahlenberg, S. G. Thacker, C. C. Berthier, C. D. Cohen, M. Kretzler, and M. J. Kaplan, “Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus,” The Journal of Immunology, vol. 187, no. 11, pp. 6143–6156, 2011.
- K. Nozawa, N. Kayagaki, Y. Tokano, H. Yagita, K. Okumura, and H. Hasimoto, “Soluble Fas (APO-1, CD95) and soluble Fas ligand in rheumatic diseases,” Arthritis & Rheumatism, vol. 40, no. 6, pp. 1126–1129, 1997.
- L. E. Munoz, C. Van Bavel, S. Franz, J. Berden, M. Herrmann, and J. van der Vlag, “Apoptosis in the pathogenesis of systemic lupus erythematosus,” Lupus, vol. 17, no. 5, pp. 371–375, 2008.
- H. Kitaura, M. Tatamiya, N. Nagata et al., “IL-18 induces apoptosis of adherent bone marrow cells in TNF-α mediated osteoclast formation in synergy with IL-12,” Immunology Letters, vol. 107, no. 1, pp. 22–31, 2006.
- T. Ohtsuki, M. J. Micallef, K. Kohno, T. Tanimoto, M. Ikeda, and M. Kurimoto, “Interleukin 18 enhances Fas ligand expression and induces apoptosis in Fas-expressing human myelomonocytic KG-1 cells,” Anticancer Research, vol. 17, no. 5A, pp. 3253–3258, 1997.
- M. Bijl, G. Horst, P. C. Limburg, and C. G. M. Kallenberg, “Fas expression on peripheral blood lymphocytes in systemic lupus erythematosus (SLE): relation to lymphocyte activation and disease activity,” Lupus, vol. 10, no. 12, pp. 866–872, 2001.
- M. Sahin, O. Aydintug, S. E. Tunc, H. Tutkak, and M. Naziroǧlu, “Serum soluble Fas levels in patients with autoimmune rheumatic diseases,” Clinical Biochemistry, vol. 40, no. 1-2, pp. 6–10, 2007.
- M. Sahebari, M. R. Hatef, Z. Rezaieyazdi, M. Abbasi, B. Abbasi, and M. Mahmoudi, “Correlation between serum levels of soluble fas (CD95/Apo-1) with disease activity in systemic lupus erythematosus patients in Khorasan, Iran,” Archives of Iranian Medicine, vol. 13, no. 2, pp. 135–142, 2010.
- J. Cheng, T. Zhou, C. Liu et al., “Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule,” Science, vol. 263, no. 5154, pp. 1759–1762, 1994.
- F. Silvestris, D. Grinello, M. Tucci, P. Cafforio, and F. Dammacco, “Enhancement of T cell apoptosis correlates with increased serum levels of soluble Fas (CD95/Apo-I) in active lupus,” Lupus, vol. 12, no. 1, pp. 8–14, 2003.
- E. Telegina, T. Reshetnyak, A. Moshnikova et al., “A possible role of Fas-ligand-mediated “reverse signaling” in pathogenesis of rheumatoid arthritis and systemic lupus erythematosus,” Immunology Letters, vol. 122, no. 1, pp. 12–17, 2009.
- F. Silvestris, P. Cafforio, M. Tucci, A. del Prete, and F. Dammacco, “VEINCTR-N, an immunogenic epitope of Fas (CD95/Apo-I), and soluble Fas enhance T-cell apoptosis in vitro. II. Functional analysis and possible implications in HIV-1 disease,” Molecular Medicine, vol. 6, no. 6, pp. 509–526, 2000.
- H. P. Carroll, V. Paunović, and M. Gadina, “Signalling, inflammation and arthritis: crossed signals: the role of interleukin-15 and -18 in autoimmunity,” Rheumatology, vol. 47, no. 9, pp. 1269–1277, 2008.
- P. Reddy, “Interleukin-18: recent advances,” Current Opinion in Hematology, vol. 11, no. 6, pp. 405–410, 2004.
- T. Dao, K. Ohashi, T. Kayano, M. Kurimoto, and H. Okamura, “Interferon-γ-inducing factor, a novel cytokine, enhances Fas ligand-mediated cytotoxicity of murine T helper 1 cells,” Cellular Immunology, vol. 173, no. 2, pp. 230–235, 1996.
- C. Shimizu, T. Fujita, Y. Fuke et al., “High circulating levels of interleukin-18 binding protein indicate the severity of glomerular involvement in systemic lupus erythematosus,” Modern Rheumatology, vol. 22, no. 1, pp. 73–79, 2012.
- E. Marín-Serrano, C. Rodríguez-Ramos, F. Diaz, L. Martín-Herrera, and J. Girón-González, “Modulation of the anti-inflammatory interleukin 10 and of proapoptotic IL-18 in patients with chronic hepatitis C treated with interferon alpha and ribavirin,” Journal of Viral Hepatitis, vol. 13, no. 4, pp. 230–234, 2006.
- H. Nakae, Y. J. Zheng, H. Wada, K. Tajimi, and S. Endo, “Involvement of IL-18 and soluble Fas in patients with postoperative hepatic failure,” European Surgical Research, vol. 35, no. 2, pp. 61–66, 2003.
- S. El-Masry, M. Lotfy, W. A. Nasif, I. M. El-Kady, and M. Al-Badrawy, “Elevated serum level of interleukin (IL)-18, interferon (IFN)-c and soluble fas in patients with pulmonary complications in tuberculosis,” Acta Microbiologica et Immunologica Hungarica, vol. 54, no. 1, pp. 65–77, 2007.
- S. Imai, N. Sato, Y. Inoue, and S. Endo, “A study of interleukin 18 and sFas in septic multiple organ dysfunction syndrome,” Journal of the Iwate Medical Association, vol. 57, no. 5, pp. 497–503, 2005.
- M. Kaizu, Y. Ami, T. Nakasone et al., “Higher levels of IL-18 circulate during primary infection of monkeys with a pathogenic SHIV than with a nonpathogenic SHIV,” Virology, vol. 313, no. 1, pp. 8–12, 2003.
- A. Sharma, A. Chakraborti, A. Das, R. K. Dhiman, and Y. Chawla, “Elevation of interleukin-18 in chronic hepatitis C: implications for hepatitis C virus pathogenesis,” Immunology, vol. 128, no. 1, part 2, pp. e514–e522, 2009.
- D. Y. Chen, T. Y. Hsieh, C. W. Hsieh, F. J. Lin, and J. L. Lan, “Increased apoptosis of peripheral blood lymphocytes and its association with interleukin-18 in patients with active untreated adult-onset Still's disease,” Arthritis Care and Research, vol. 57, no. 8, pp. 1530–1538, 2007.
- M. Sahebari, Z. Rezaieyazdi, M. J. Nakhjavani, M. Hatef, M. Mahmoudi, and S. Akhlaghi, “Correlation between serum concentrations of soluble Fas (CD95/Apo-1) and IL-18 in patients with systemic lupus erythematosus,” Rheumatology International, vol. 32, no. 3, pp. 601–606, 2012.
- P. Y. Tsai, S. M. Ka, J. M. Chang, et al., “Antroquinonol differentially modulates T cells activity, reduces IL-18 production, but enhances Nrf2 activation in accelerated severe lupus nephritis,” Arthritis & Rheumatism, vol. 64, no. 1, pp. 232–242, 2012.
- J. Faust, J. Menke, J. Kriegsmann et al., “Correlation of renal tubular epithelial cell-derived interleukin-18 up-regulation with disease activity in MRL-Faslpr mice with autoimmune lupus nephritis,” Arthritis & Rheumatism, vol. 46, no. 11, pp. 3083–3095, 2002.
- J. H. Hao, D. Q. Ye, G. Q. Zhang et al., “Elevated levels of serum soluble Fas are associated with organ and tissue damage in systemic lupus erythematosus among Chinese,” Archives of Dermatological Research, vol. 297, no. 7, pp. 329–332, 2006.
- N. A. Fathi, M. R. Hussein, H. I. Hassan, E. Mosad, H. Galal, and N. A. Afifi, “Glomerular expression and elevated serum Bcl-2 and Fas proteins in lupus nephritis: preliminary findings,” Clinical and Experimental Immunology, vol. 146, no. 2, pp. 339–343, 2006.
- C. Miret, J. Font, R. Molina et al., “Relationship of oncogenes (sFas, Bcl-2) and cytokines (IL-10, alfa-TNF) with the activity of systemic lupus erythematosus,” Anticancer Research, vol. 21, no. 4B, pp. 3053–3059, 2001.
- E. M. Tan, A. S. Cohen, and J. F. Fries, “The 1982 revised criteria for the classification of systemic lupus erythrematosus,” Arthritis & Rheumatism, vol. 25, no. 11, pp. 1271–1277, 1982.
- M. A. Dalboni, C. Sardenberg, M. C. Andreoli et al., “Soluble Fas: a novel marker of inflammation in uremia,” Artificial Organs, vol. 27, no. 8, pp. 687–691, 2003.
- G. C. Tsokos, “Systemic lupus erythematosus,” The New England Journal of Medicine, vol. 365, no. 22, pp. 2110–2121, 2011.
- D. Liang, W. Ma, C. Yao, H. Liu, and X. Chen, “Imbalance of interleukin 18 and interleukin 18 binding protein in patients with lupus nephritis,” Cellular & Molecular Immunology, vol. 3, no. 4, pp. 303–306, 2006.
- N. Calvani, H. B. Richards, M. Tucci, G. Pannarale, and F. Silvestris, “Up-regulation of IL-18 and predominance of a Th1 immune response is a hallmark of lupus nephritis,” Clinical and Experimental Immunology, vol. 138, no. 1, pp. 171–178, 2004.
- T. Tsukinoki, H. Sugiyama, R. Sunami et al., “Mesangial cell Fas ligand: upregulation in human lupus nephritis and NF-κB-mediated expression in cultured human mesangial cells,” Clinical and Experimental Nephrology, vol. 8, no. 3, pp. 196–205, 2004.