Anti-tumor necrosis factor-alpha antibody treatment reduces serum CXCL16 levels in patients with rheumatoid arthritis
Autor: | Eiji Torikai, Yasunori Kageyama, Akira Nagano |
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Rok vydání: | 2006 |
Předmět: |
Male
musculoskeletal diseases medicine.medical_specialty Chemokine Prednisolone Immunology Anti-Inflammatory Agents Gastroenterology Arthritis Rheumatoid Rheumatology immune system diseases Internal medicine medicine Humans Immunologic Factors Immunology and Allergy CXCL10 skin and connective tissue diseases CX3CL1 CXCL16 Receptors Scavenger biology Chemokine CX3CL1 business.industry Antibodies Monoclonal Chemokine CXCL16 Middle Aged medicine.disease Infliximab Chemokine CXCL10 stomatognathic diseases Rheumatoid arthritis biology.protein Drug Therapy Combination Female Antibody business Chemokines CXC medicine.drug |
Zdroj: | Rheumatology International. 27:467-472 |
ISSN: | 1437-160X 0172-8172 |
Popis: | 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. |
Databáze: | OpenAIRE |
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