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interleukin-6 and chronic inflammation白细胞介素- 6和慢性炎症
Available online /content/8/S2/S3
Proceedings
Interleukin-6 and chronic inflammation
Cem Gabay
Division of Rheumatology, University Hospital of Geneva, and Department of Pathology and Immunology, University of Geneva School of Medicine,
Geneva, Switzerland
Corresponding author: Cem Gabay, cem.gabay@hcuge.ch
Published: 28 July 2006 Arthritis Research Therapy 2006, 8(Suppl 2):S3
This article is online at /content/8/S2/S3 (doi:10.1186/ar1917)
© 2006 BioMed Central Ltd
Abstract acute phase proteins (Figure 1), as well as numerous
Interleukin (IL)-6 is produced at the site of inflammation and plays a behavioural, physiological, biochemical and nutritional
key role in the acute phase response as defined by a variety of changes [4]. The acute phase proteins have been defined as
clinical and biological features such as the production of acute a set of plasma proteins with concentrations that increase
phase proteins. IL-6 in combination with its soluble receptor (positive acute phase proteins) or decrease (negative acute
sIL-6Rα, dictates the transition from acute to chonic inflammation phase proteins) by at least 25% in inflammatory disorders
by changing the nature of leucocyte infiltrate (from polymorpho- [4,5] (Figure 1). The changes in concentrations of acute
nuclear neutrophils to monocyte/macrophages). In addition, IL-6
exerts stimulatory effects on T- and B-cells, thus favoring chronic phase proteins are largely due to changes in their production
inflammatory responses.
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