The expression of IL-20 and IL-24 and their shared receptors are increased in rheumatoid arthritis and spondyloarthropathy

被引：97

作者：

Kragstrup, Tue Wenzel ^{[1
]}

Otkjaer, Kristian ^{[2
]}

Hohn, Christian ^{[1
]}

Jorgensen, Annette ^{[3
]}

Hokland, Marianne ^{[1
]}

Iversen, Lars ^{[2
]}

Deleuran, Bent ^{[1
,3
]}

机构：

[1] Aarhus Univ, Inst Med Microbiol & Immunol, DK-8000 Aarhus, Denmark

[2] Aarhus Univ Hosp, Dept Dermato Venerol, DK-8000 Aarhus, Denmark

[3] Aarhus Univ Hosp, Dept Rheumatol, DK-8000 Aarhus, Denmark

来源：

CYTOKINE | 2008年 / 41卷 / 01期

关键词：

IL-20; IL-24; arthritis;

D O I：

10.1016/j.cyto.2007.10.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

The purpose of this study was to analyze the expression of the two proinflammatory cytokines IL-20 and IL-24 and their shared receptors in rheumatoid arthritis and spondyloarthropathy. IL-20 was increased in plasma of rheumatoid arthritis patients compared with osteoarthritis patients and IL-24 was increased in synovial fluid and plasma of rheumatoid arthritis and spondyloarthropathy patients compared with osteoarthritis patients. IL-20 and IL-24 mRNA was only present at low levels in the synovium. In the synovial membrane, IL-20 protein was present in mononuclear cells and neutrophil granulocytes whereas IL-24 protein was observed in endothelial cells and mononuclear cells. IL-20 receptor type I and IL-22 receptor were expressed by granulocytes in the synovial fluid. In synovial fluid mononuclear cell cultures, stimulation with recombinant human IL-20 or recombinant human IL-24 induced monocyte chemoattractant protein I (CCL2/MCP-1) secretion, but not tumour necrosis factor alpha mRNA synthesis or IL-6 secretion. Both IL-20 and IL-24 showed correlations to CCL2/MCP-1 in plasma from rheumatoid arthritis and spondyloarthropathy patients. This study associates IL-20 and IL-24 to the synovium of rheumatoid arthritis and spondyloarthropathy and results indicate that the two cytokines contribute to disease pathogenesis through recruitment of neutrophil granulocytes and induction of CCL2/MCP-1. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：16 / 23

页数：8

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