Anti-tumor necrosis factor-alpha antibody treatment reduces serum CXCL16 levels in patients with rheumatoid arthritis

被引：41

作者：

Kageyama, Yasunori ^{[1
]}

Torikai, Eiji ^{[1
]}

Nagano, Akira ^{[1
]}

机构：

[1] Hamamatsu Univ Sch Med, Dept Orthopaed Surg, Hamamatsu, Shizuoka 4313192, Japan

来源：

RHEUMATOLOGY INTERNATIONAL | 2007年 / 27卷 / 05期

关键词：

infliximab; CXCL16; fractalkine; interferon-gamma inducible protein-10; rheumatoid arthritis;

D O I：

10.1007/s00296-006-0241-1

中图分类号：

R5 [内科学];

学科分类号：

1002 [临床医学]; 100201 [内科学];

摘要：

The aim of this study was to analyze the change of serum chemokins levels of CXCL16, CX3CL1/Fractalkine, and CXCL10/interferon-gamma inducible protein-10 (IP-10) with rheumatoid arthritis (RA), by infliximab treatment. The effects of infliximab treatment were studied in 23 patients with RA, over a period of 30 weeks. The serum levels of CXCL16, Fractalkine, and IP-10, were measured at the baseline, just before initial treatment, and at 14 and 30 weeks after the initial treatment, with infliximab by ELISA. The higher levels of serum CXCL16 in the RA patients before treatment with infliximab significantly decreased at 14 and 30 weeks after the initial treatment with infliximab, but the serum Fractalkine and IP-10 levels did not decrease significantly. Infliximab treatment significantly lowered the serum levels of CXCL16 in patients with RA. CXCL16 is one of the crucial chemokines regulated by infliximab treatment.

引用

页码：467 / 472

页数：6

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