Skip to main content
Erschienen in: Clinical Rheumatology 3/2007

01.03.2007 | Original Article

Elevated levels of soluble Fas (APO-1, CD95), soluble Fas ligand, and matrix metalloproteinase-3 in sera from patients with active untreated adult onset Still’s disease

verfasst von: Der-Yuan Chen, Joung-Liang Lan, Fang-Ju Lin, Tsu-Yi Hsieh

Erschienen in: Clinical Rheumatology | Ausgabe 3/2007

Einloggen, um Zugang zu erhalten

Abstract

To investigate serum levels of soluble Fas (sFas), soluble Fas ligand (sFas-L), and matrix metalloproteinase-3 (MMP-3) in patients with active untreated adult onset Still’s disease (AOSD). Serum levels of sFas, sFas-L, and MMP-3 were determined by enzyme-linked immunosorbent assays in 20 patients with active untreated AOSD, 20 patients with active rheumatoid arthritis (RA), and 20 healthy controls. Linear regression was used to evaluate the correlation between clinical activity scores and serum levels of sFas, sFas-L, and MMP-3 in AOSD patients. Significantly higher levels of sFas, sFas-L, and MMP-3 in sera were found in active untreated AOSD patients compared to healthy controls. Serum levels of sFas, sFas-L, and MMP-3 correlated well with clinical activity scores of AOSD patients (r=0.467, 0.694, and 0.798, respectively). There was a significant correlation between CRP values and serum levels of sFas-L as well as MMP-3 (r=0.583 and r=0.582, respectively, both p<0.01), and a positive correlation between serum sFas-L levels and serum MMP-3 levels (r=0.726, p<0.001) in AOSD patients. Significantly higher levels of serum sFas-L were found in AOSD patients than in RA patients. Serum levels of sFas, sFas-L, and MMP-3 fluctuated and were found to be parallel to disease activity of AOSD. sFas, sFas-L, and MMP-3, which were significantly elevated in sera of active untreated AOSD patients and paralleled disease activity, may be involved in the pathogenesis of this disease. Further studies are needed to determine the pathophysiologic role of sFas, sFas-L, and MMP-3 in AOSD.
Literatur
2.
Zurück zum Zitat Ohta A, Yamaguchi M, Kaneoka H, Nagayoshi T, Hiida M (1987) Adult Still’s disease: review of 228 cases from the literature. J Rheumatol 14:1139–1146PubMed Ohta A, Yamaguchi M, Kaneoka H, Nagayoshi T, Hiida M (1987) Adult Still’s disease: review of 228 cases from the literature. J Rheumatol 14:1139–1146PubMed
3.
Zurück zum Zitat Chen DY, Lan JL, Lin FJ, Hsieh TY, Wen MC (2004) A predominance of Th1 cytokine in peripheral blood and pathological tissues of patients with active untreated adult-onset Still’s disease. Ann Rheum Dis 63:1300–1306PubMedCrossRef Chen DY, Lan JL, Lin FJ, Hsieh TY, Wen MC (2004) A predominance of Th1 cytokine in peripheral blood and pathological tissues of patients with active untreated adult-onset Still’s disease. Ann Rheum Dis 63:1300–1306PubMedCrossRef
4.
Zurück zum Zitat Ramsdell F, Seaman MS, Miller RE, Picha KS, Kennedy MK, Lynch DH (1994) Differential ability of Th1 and Th2 cells to express Fas ligand and to undergo activation-induced cell death. Int Immunol 6:1545–1553PubMedCrossRef Ramsdell F, Seaman MS, Miller RE, Picha KS, Kennedy MK, Lynch DH (1994) Differential ability of Th1 and Th2 cells to express Fas ligand and to undergo activation-induced cell death. Int Immunol 6:1545–1553PubMedCrossRef
5.
Zurück zum Zitat Zhang X, Brunner T, Carter L, Dutton RW, Rogers P, Bradley L et al (1997) Unequal death in T helper cell (Th)1 and Th2 effectors: Th1, but not Th2, effectors undergo rapid Fas/FasL-mediated apoptosis. J Exp Med 185:1837–1849PubMedCrossRef Zhang X, Brunner T, Carter L, Dutton RW, Rogers P, Bradley L et al (1997) Unequal death in T helper cell (Th)1 and Th2 effectors: Th1, but not Th2, effectors undergo rapid Fas/FasL-mediated apoptosis. J Exp Med 185:1837–1849PubMedCrossRef
6.
Zurück zum Zitat Chen DY, Lan JL, Lin FJ, Hsieh TY (2004) Proinflammatory cytokine profiles in the sera and in the pathological tissues of patients with active untreated adult onset Still’s disease. J Rheumatol 31:2189–2198PubMed Chen DY, Lan JL, Lin FJ, Hsieh TY (2004) Proinflammatory cytokine profiles in the sera and in the pathological tissues of patients with active untreated adult onset Still’s disease. J Rheumatol 31:2189–2198PubMed
7.
Zurück zum Zitat Choi JH, Suh CH, Lee YM, Suh YJ, Lee SK, Kim SS et al (2003) Serum cytokine profiles in patients with adult onset Still’s disease. J Rheumatol 30:2422–2427PubMed Choi JH, Suh CH, Lee YM, Suh YJ, Lee SK, Kim SS et al (2003) Serum cytokine profiles in patients with adult onset Still’s disease. J Rheumatol 30:2422–2427PubMed
8.
Zurück zum Zitat Kawashima M, Yamamura M, Taniai M, Yamauchi H, Tanimoto T, Kurimoto M et al (2001) Levels of interleukin-18 and its binding inhibitors in the blood circulation of patients with adult-onset Still’s disease. Arthritis Rheum 44:550–560PubMedCrossRef Kawashima M, Yamamura M, Taniai M, Yamauchi H, Tanimoto T, Kurimoto M et al (2001) Levels of interleukin-18 and its binding inhibitors in the blood circulation of patients with adult-onset Still’s disease. Arthritis Rheum 44:550–560PubMedCrossRef
9.
Zurück zum Zitat Ohtsuki T, Micallef MJ, Kohno K, Tanimoto T, Ikeda M, Kurimoto M (1997) Interleukin 18 enhances Fas ligand expression and induces apoptosis in Fas-expressing human myelomonocytic KG-1 cells. Anticancer Res 17(5A):3253–3258PubMed Ohtsuki T, Micallef MJ, Kohno K, Tanimoto T, Ikeda M, Kurimoto M (1997) Interleukin 18 enhances Fas ligand expression and induces apoptosis in Fas-expressing human myelomonocytic KG-1 cells. Anticancer Res 17(5A):3253–3258PubMed
11.
Zurück zum Zitat Van Parijs L, Abbas Ak (1998) Homeostasis and self-tolerance in the immune system: turning lymphocytes off. Science 280:243–248PubMedCrossRef Van Parijs L, Abbas Ak (1998) Homeostasis and self-tolerance in the immune system: turning lymphocytes off. Science 280:243–248PubMedCrossRef
12.
Zurück zum Zitat Funauchi M, Sugiyama M, SukYoo B, Ikoma S, Ohno M, Kinoshita K et al (2001) A possible role of apoptosis for regulating autoreactive response in systemic lupus erythematosus. Lupus 10:284–288PubMedCrossRef Funauchi M, Sugiyama M, SukYoo B, Ikoma S, Ohno M, Kinoshita K et al (2001) A possible role of apoptosis for regulating autoreactive response in systemic lupus erythematosus. Lupus 10:284–288PubMedCrossRef
14.
Zurück zum Zitat Suda T, Takahasi T, Golstain P, Nagata S (1993) Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell 75:1169–1178PubMedCrossRef Suda T, Takahasi T, Golstain P, Nagata S (1993) Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell 75:1169–1178PubMedCrossRef
15.
Zurück zum Zitat Suda T, Okazaki T, Naito Y, Yokota T, Arai N, Ozaki S et al (1995) Expression of the Fas ligand in cells of T cell lineage. J Immunol 154:3806–3813PubMed Suda T, Okazaki T, Naito Y, Yokota T, Arai N, Ozaki S et al (1995) Expression of the Fas ligand in cells of T cell lineage. J Immunol 154:3806–3813PubMed
16.
Zurück zum Zitat Ju ST, Panka DJ, Cui H, Ettinger R, El-Khatib M, Sherr DH et al (1995) Fas (CD95)/FasL interactions required for programmed cell death after T-cell activation. Nature 373:444–448PubMedCrossRef Ju ST, Panka DJ, Cui H, Ettinger R, El-Khatib M, Sherr DH et al (1995) Fas (CD95)/FasL interactions required for programmed cell death after T-cell activation. Nature 373:444–448PubMedCrossRef
17.
18.
Zurück zum Zitat Ito RM, Terasaki S, Itoh J, Katoh H, Yonehara S, Nose M et al (1997) Rheumatic diseases in an MRL strain of mice with a deficit in the functional Fas ligand. Arthritis Rheum 40:1054–1063PubMed Ito RM, Terasaki S, Itoh J, Katoh H, Yonehara S, Nose M et al (1997) Rheumatic diseases in an MRL strain of mice with a deficit in the functional Fas ligand. Arthritis Rheum 40:1054–1063PubMed
19.
Zurück zum Zitat Watanabe-Fukunaga R, Brannan CI, Copeland NG, Jenkins NA, Nagata S (1992) Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature 356:314–317PubMedCrossRef Watanabe-Fukunaga R, Brannan CI, Copeland NG, Jenkins NA, Nagata S (1992) Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature 356:314–317PubMedCrossRef
20.
Zurück zum Zitat Sneller MC, Wang J, Dale JK, Strober W, Middelton LA, Choi Y et al (1997) Clinical, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis. Blood 89:1341–1348PubMed Sneller MC, Wang J, Dale JK, Strober W, Middelton LA, Choi Y et al (1997) Clinical, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis. Blood 89:1341–1348PubMed
21.
Zurück zum Zitat Mountz JD, Zhou T, Su X, Wu J, Cheng J (1996) The role of programmed cell death as autoimmune disease. Clin Immunol Immunopathol 80:S2–S14PubMedCrossRef Mountz JD, Zhou T, Su X, Wu J, Cheng J (1996) The role of programmed cell death as autoimmune disease. Clin Immunol Immunopathol 80:S2–S14PubMedCrossRef
22.
23.
Zurück zum Zitat Papoff G, Cascino I, Eramo A, Starace G, Lynch DH, Ruberti G (1996) An N-terminal domain shared by Fas/Apo-1 (CD95) soluble variants prevent cell death in vitro. J Immunol 156:4622–4630PubMed Papoff G, Cascino I, Eramo A, Starace G, Lynch DH, Ruberti G (1996) An N-terminal domain shared by Fas/Apo-1 (CD95) soluble variants prevent cell death in vitro. J Immunol 156:4622–4630PubMed
24.
Zurück zum Zitat Cheng J, Zhou T, Liu C (1994) Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. Science 263:1759–1762PubMedCrossRef Cheng J, Zhou T, Liu C (1994) Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. Science 263:1759–1762PubMedCrossRef
25.
Zurück zum Zitat Silvestris F, Williams RC, Calvani N, Grinello D, Tucci M, Cafforio P et al (2002) Serum elevations of soluble Fas (CD95/Apo-1) concur in deregulating T cell apoptosis during active lupus disease. Clin Exp Med 2:13–27PubMedCrossRef Silvestris F, Williams RC, Calvani N, Grinello D, Tucci M, Cafforio P et al (2002) Serum elevations of soluble Fas (CD95/Apo-1) concur in deregulating T cell apoptosis during active lupus disease. Clin Exp Med 2:13–27PubMedCrossRef
26.
Zurück zum Zitat Kayagaki N, Kawasaki A, Ebata T, Ohmoto H, Ikeda S, Inoue K et al (1995) Metalloproteinase-mediated release of human Fas ligand. J Exp Med 182:1777PubMedCrossRef Kayagaki N, Kawasaki A, Ebata T, Ohmoto H, Ikeda S, Inoue K et al (1995) Metalloproteinase-mediated release of human Fas ligand. J Exp Med 182:1777PubMedCrossRef
27.
Zurück zum Zitat Matsuno H, Yudoh K, Watanabe Y, Nakazawa F, Aono H, Kimura T (2001) Stromelysin-1 (MMP-3) in synovial fluid of patients with rheumatoid arthritis has potential to cleave membrane bound Fas ligand. J Rheumatol 28:22–28PubMed Matsuno H, Yudoh K, Watanabe Y, Nakazawa F, Aono H, Kimura T (2001) Stromelysin-1 (MMP-3) in synovial fluid of patients with rheumatoid arthritis has potential to cleave membrane bound Fas ligand. J Rheumatol 28:22–28PubMed
28.
Zurück zum Zitat Tanaka M, Suda T, Takahasi T, Nagata S (1995) Expression of the functional soluble form of human Fas ligand in activated lymphocyte. EMBO J 14:1129–1136PubMed Tanaka M, Suda T, Takahasi T, Nagata S (1995) Expression of the functional soluble form of human Fas ligand in activated lymphocyte. EMBO J 14:1129–1136PubMed
29.
Zurück zum Zitat Nozawa K, Kayagaki N, Tokano Y, Yagita H, Okumura K, Hasimoto H (1997) Soluble Fas (APO-1, CD95) and soluble Fas ligand in rheumatic diseases. Arthritis Rheum 40:1126–1129PubMed Nozawa K, Kayagaki N, Tokano Y, Yagita H, Okumura K, Hasimoto H (1997) Soluble Fas (APO-1, CD95) and soluble Fas ligand in rheumatic diseases. Arthritis Rheum 40:1126–1129PubMed
30.
Zurück zum Zitat Christensson M, Pettersson E, Eneslatt K, Christensson B, Bratt J, Rantapaa-Dahlqvist S et al (2002) Serum sFas levels are elevated in ANCA-positive vasculitis compared with other autoimmune diseases. J Clin Immunol 22:220–227PubMedCrossRef Christensson M, Pettersson E, Eneslatt K, Christensson B, Bratt J, Rantapaa-Dahlqvist S et al (2002) Serum sFas levels are elevated in ANCA-positive vasculitis compared with other autoimmune diseases. J Clin Immunol 22:220–227PubMedCrossRef
31.
Zurück zum Zitat Emmenegger U, Zehnder R, Frey U, Reimers A, Spaeth PJ, Neftel KA (2000) Elevation of soluble Fas and soluble Fas ligand in reactive macrophage activation syndromes. Am J Hematol 64:116–119PubMedCrossRef Emmenegger U, Zehnder R, Frey U, Reimers A, Spaeth PJ, Neftel KA (2000) Elevation of soluble Fas and soluble Fas ligand in reactive macrophage activation syndromes. Am J Hematol 64:116–119PubMedCrossRef
32.
Zurück zum Zitat Yamaguchi M, Ohta A, Tsunematsu T, Kasukawa R, Mizushima Y, Kashiwagi S et al (1992) Preliminary criteria for classification of adult Still’s disease. J Rheumatol 19:424–430PubMed Yamaguchi M, Ohta A, Tsunematsu T, Kasukawa R, Mizushima Y, Kashiwagi S et al (1992) Preliminary criteria for classification of adult Still’s disease. J Rheumatol 19:424–430PubMed
33.
Zurück zum Zitat Pouchot J, Sampalis JS, Beaudet F, Carette S, Decary F, Salusinsky-Sternbach M et al (1991) Adult Still’s disease: manifestations, disease course, and outcome in 62 patients. Medicine 70:118–136PubMedCrossRef Pouchot J, Sampalis JS, Beaudet F, Carette S, Decary F, Salusinsky-Sternbach M et al (1991) Adult Still’s disease: manifestations, disease course, and outcome in 62 patients. Medicine 70:118–136PubMedCrossRef
34.
Zurück zum Zitat Arnett FC, Edworthy SM, Bloch DA et al (1988) The american rheumatism association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31:315–324PubMed Arnett FC, Edworthy SM, Bloch DA et al (1988) The american rheumatism association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31:315–324PubMed
35.
Zurück zum Zitat Li NL, Nie H, Yu QW, Zhang JY, Ma AL, Shen BH et al (2004) Role of soluble Fas ligand in autoimmune diseases. World J Gastroenterol 10:3151–3156PubMed Li NL, Nie H, Yu QW, Zhang JY, Ma AL, Shen BH et al (2004) Role of soluble Fas ligand in autoimmune diseases. World J Gastroenterol 10:3151–3156PubMed
36.
Zurück zum Zitat Suda T, Hashimoto H, Tanaka M, Ochi T, Nagata S (1997) Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing. J Exp Med 186:2045–2050PubMedCrossRef Suda T, Hashimoto H, Tanaka M, Ochi T, Nagata S (1997) Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing. J Exp Med 186:2045–2050PubMedCrossRef
37.
Zurück zum Zitat Kim S, Kim JY, Lee TH, Suk K, Cha HS, Koh EM et al (2002) Soluble Fas ligand-susceptible “memory” cells in human but not in mice: potential role of soluble Fas ligand in deletion of auto-reactive cells. Autoimmunity 35:15–20PubMedCrossRef Kim S, Kim JY, Lee TH, Suk K, Cha HS, Koh EM et al (2002) Soluble Fas ligand-susceptible “memory” cells in human but not in mice: potential role of soluble Fas ligand in deletion of auto-reactive cells. Autoimmunity 35:15–20PubMedCrossRef
38.
Zurück zum Zitat Chen JJ, Sun Y, Nabel GJ (1998) Regulation of the proinflammatory effects of Fas ligand (CD95L). Science 282:1714–1717PubMedCrossRef Chen JJ, Sun Y, Nabel GJ (1998) Regulation of the proinflammatory effects of Fas ligand (CD95L). Science 282:1714–1717PubMedCrossRef
39.
Zurück zum Zitat Szodoray P, Jellestad S, Nakken B, Brun JG, Jonsson R (2003) Programmed cell death in rheumatoid arthritis peripheral blood T-cell subpopulations determined by laser scanning cytometry. Lab Invest 83:1839–1848PubMedCrossRef Szodoray P, Jellestad S, Nakken B, Brun JG, Jonsson R (2003) Programmed cell death in rheumatoid arthritis peripheral blood T-cell subpopulations determined by laser scanning cytometry. Lab Invest 83:1839–1848PubMedCrossRef
40.
Zurück zum Zitat Nishioka K, Hasusuma T, Kato T, Sumida T, Kobata T (1998) Apoptosis in rheumatoid arthritis: a novel pathway in the regulation of synovial tissue. Arthritis Rheum 41:1–9PubMedCrossRef Nishioka K, Hasusuma T, Kato T, Sumida T, Kobata T (1998) Apoptosis in rheumatoid arthritis: a novel pathway in the regulation of synovial tissue. Arthritis Rheum 41:1–9PubMedCrossRef
41.
Zurück zum Zitat Chou CT, Yang JS, Lee MR (2001) Apoptosis in rheumatoid arthritis-expression of Fas, Fas-L, p53, and Bcl-2 in rheumatoid synovial tissues. J Pathol 193:110–116PubMedCrossRef Chou CT, Yang JS, Lee MR (2001) Apoptosis in rheumatoid arthritis-expression of Fas, Fas-L, p53, and Bcl-2 in rheumatoid synovial tissues. J Pathol 193:110–116PubMedCrossRef
42.
Zurück zum Zitat Werb A, Alexander CM (1993) Proteinases and matric degradation. In: Kelley WN, Harris ED, Ruddy S, Sledge CB (eds) Textbook of rheumatology, 4th edn. Saunders, Philadelphia Werb A, Alexander CM (1993) Proteinases and matric degradation. In: Kelley WN, Harris ED, Ruddy S, Sledge CB (eds) Textbook of rheumatology, 4th edn. Saunders, Philadelphia
43.
Zurück zum Zitat Green MJ, Gough AKS, Devlin J, Smith J, Astin P, Taylor D et al (2003) Serum MMP-3 and MMP-1 and progression of joint damage in early rheumatoid arthritis. Rheumatology 42:83–88PubMedCrossRef Green MJ, Gough AKS, Devlin J, Smith J, Astin P, Taylor D et al (2003) Serum MMP-3 and MMP-1 and progression of joint damage in early rheumatoid arthritis. Rheumatology 42:83–88PubMedCrossRef
44.
Zurück zum Zitat Katrib A, Smith MD, Ahern MJ, Slavotinek J, Stafford L, Cuello C et al (2003) Reduced chemokine and matrix metalloproteinase expression in patients with rheumatoid arthritis achieving remission. J Rheumatol 30:10–21PubMed Katrib A, Smith MD, Ahern MJ, Slavotinek J, Stafford L, Cuello C et al (2003) Reduced chemokine and matrix metalloproteinase expression in patients with rheumatoid arthritis achieving remission. J Rheumatol 30:10–21PubMed
Metadaten
Titel
Elevated levels of soluble Fas (APO-1, CD95), soluble Fas ligand, and matrix metalloproteinase-3 in sera from patients with active untreated adult onset Still’s disease
verfasst von
Der-Yuan Chen
Joung-Liang Lan
Fang-Ju Lin
Tsu-Yi Hsieh
Publikationsdatum
01.03.2007
Verlag
Springer-Verlag
Erschienen in
Clinical Rheumatology / Ausgabe 3/2007
Print ISSN: 0770-3198
Elektronische ISSN: 1434-9949
DOI
https://doi.org/10.1007/s10067-006-0378-z

Weitere Artikel der Ausgabe 3/2007

Clinical Rheumatology 3/2007 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.