Serum interleukin 18 and tumour necrosis factor-α levels are increased in Behcet's disease

Summary Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T‐helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)‐18 and tumour necrosis factor (TNF)‐α levels of patients with Behcet's disease. Twenty‐seven patients...

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Published inClinical and experimental dermatology Vol. 30; no. 1; pp. 61 - 63
Main Authors Oztas, M. O., Onder, M., Gurer, M. A., Bukan, N., Sancak, B.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.01.2005
Blackwell
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Online AccessGet full text
ISSN0307-6938
1365-2230
DOI10.1111/j.1365-2230.2004.01684.x

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Abstract Summary Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T‐helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)‐18 and tumour necrosis factor (TNF)‐α levels of patients with Behcet's disease. Twenty‐seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL‐18 and TNF‐α level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL‐18 and TNF‐α levels of Behcet patients (rs = 0.627, P < 0.0001). IL‐18 and TNF‐α levels may be related to disease pathogenesis. Increased levels of IL‐18 also support Th1 predominance in Behcet's disease.
AbstractList Summary Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T‐helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)‐18 and tumour necrosis factor (TNF)‐α levels of patients with Behcet's disease. Twenty‐seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL‐18 and TNF‐α level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL‐18 and TNF‐α levels of Behcet patients (rs = 0.627, P < 0.0001). IL‐18 and TNF‐α levels may be related to disease pathogenesis. Increased levels of IL‐18 also support Th1 predominance in Behcet's disease.
Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)-18 and tumour necrosis factor (TNF)-alpha levels of patients with Behcet's disease. Twenty-seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL-18 and TNF-alpha level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL-18 and TNF-alpha levels of Behcet patients (rs = 0.627, P < 0.0001). IL-18 and TNF-alpha levels may be related to disease pathogenesis. Increased levels of IL-18 also support Th1 predominance in Behcet's disease.Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)-18 and tumour necrosis factor (TNF)-alpha levels of patients with Behcet's disease. Twenty-seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL-18 and TNF-alpha level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL-18 and TNF-alpha levels of Behcet patients (rs = 0.627, P < 0.0001). IL-18 and TNF-alpha levels may be related to disease pathogenesis. Increased levels of IL-18 also support Th1 predominance in Behcet's disease.
Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)-18 and tumour necrosis factor (TNF)-alpha levels of patients with Behcet's disease. Twenty-seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL-18 and TNF-alpha level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL-18 and TNF-alpha levels of Behcet patients (rs = 0.627, P < 0.0001). IL-18 and TNF-alpha levels may be related to disease pathogenesis. Increased levels of IL-18 also support Th1 predominance in Behcet's disease.
Author Bukan, N.
Gurer, M. A.
Sancak, B.
Oztas, M. O.
Onder, M.
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Issue 1
Keywords Human
Skin disease
Stomatology
Dermatology
Cardiovascular disease
Behçet syndrome
Genital diseases
Interleukin 18
Vascular disease
Eye disease
Vasculitis
Systemic disease
Serum
Tumor necrosis factor α
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References_xml – reference: Aeberli D, Oertle S, Mauron H et al. Inhibition of the TNF-pathway: use of infliximab and etanercept as remission-inducing agents in cases of therapy-resistant chronic inflammatory disorders. Swiss Med Wkly 2002; 32: 414-22.
– reference: Taniguchi M, Nagaoka K, Kunikata T et al. Characterization of antihuman interleukin-18 (IL-18) interferon-gamma-inducing factor (IGIF) mononclonal antibodies and their application in the measurement of human IL-18 by ELISA. J Immunol Methods 1997; 206: 107-13.DOI: 10.1016/S0022-1759(97)00094-X
– reference: Kosar A, Haznedaroglu S, Karaaslan Y et al. Effects of interferon-alpha2a treatment on serum levels of tumour necrosis factor-alpha, tumour necrosis factor-alpha2 receptor, interleukin-2, interleukin-2 receptor, and E-selectin in Behcet's disease. Rheumatol Int 1999; 19: 11-4.DOI: 10.1007/s002960050091
– reference: Ahmad T, Wallace GR, James T et al. Mapping the HLA association in Behcet's disease: a role for tumour necrosis factor polymorphisms? Arthritis Rheum 2003; 48: 807-13.DOI: 10.1002/art.10815
– reference: Criteria for diagnosis of Behcet's disease. International Study Group for Behcet's disease. Lancet 1990; 335: 1078-80.
– reference: Gul A. Behcet's disease: an update on the pathogenesis. Clin Exp Rheumatol 2001; 19: S6-12.
– reference: Turan B, Gallati H, Erdi H et al. Systemic levels of the T cell regulatory cytokines IL-10 and IL-12 in Behcet's disease; soluble TNFR-75 as a biological marker of disease activity. J Rheumatol 1997; 24: 128-32.
– reference: Hamzaoui K, Hamzaoui A, Guemira F et al. Cytokine profile in Behcet's disease patients. Relationship with disease activity. Scand J Rheumatol 2002; 31: 205-10.DOI: 10.1080/030097402320318387
– reference: Behcet H. Ueber rezidiverende aphtoese, durch ein virus verur sachte Geschwuere am mund am Auge und an den Genitalien. Dermatol Wochenschr 1937; 105: 1152.
– reference: Engelberts I, Moller A, Schoen GJ et al. Evaluation of measurement of human TNF in plasma by ELISA. Lymphokine Cytokine Res 1991; 10: 69-76.
– reference: Ghayur T, Banerjee S, Hugunin M et al. Caspase-1 processes IFN-gamma-inducing factor and regulates LPS-induced IFN-gamma production. Nature 1997; 386: 619-23.DOI: 10.1038/386619a0
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Snippet Summary Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T‐helper type 1 (Th1) lymphocytes. In this study, we tried to...
Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. In this study, we tried to determine...
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SubjectTerms Adult
Behcet Syndrome - blood
Biological and medical sciences
Enzyme-Linked Immunosorbent Assay
Female
Humans
Interleukin-18 - blood
Male
Medical sciences
Middle Aged
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Tumor Necrosis Factor-alpha - metabolism
Title Serum interleukin 18 and tumour necrosis factor-α levels are increased in Behcet's disease
URI https://api.istex.fr/ark:/67375/WNG-PC1MKG23-Z/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1365-2230.2004.01684.x
https://www.ncbi.nlm.nih.gov/pubmed/15663506
https://www.proquest.com/docview/67367594
Volume 30
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