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- Title
The effect of infliximab on chemokines in patients with rheumatoid arthritis.
- Authors
Torikai, Eiji; Kageyama, Yasunori; Suzuki, Motohiro; Ichikawa, Tetsuya; Nagano, Akira
- Abstract
Rheumatoid arthritis (RA) is an autoimmune disease characterized by infiltration of lymphocytes, macrophages, and plasma cells into synovial membrane. The chemokines family promotes chemotactic activity in various leukocyte cell types. Chemokines thus play an essential role in the pathological formation of RA. The aim of the present study was to evaluate the influence of infliximab on serum levels of various chemokines. Twenty-four RA patients were involved in this study, which took place between March 2003 and February 2006. Infliximab was administered by intravenous infusion at a dosage of 3 mg/kg. All patients underwent general and physical examinations and routine blood and urinary analysis at the baseline, at 14 weeks, and at 30 weeks after the initial treatment. To determine whether serum and synovial fluid from RA also contained significant levels of chemokines compared with osteoarthritis patients (OA), GRO-α, MIP-1α, MIP-1β and regulated on activation normal T cell expressed and secreted (RANTES) levels of serum and synovial fluid were measured by ELISA in 20 RA patients and 20 OA patients. GRO-α, MIP-1β, and RANTES levels were significantly higher in RA compared with normal volunteers, while MIP-1α levels showed no significant differences. The mean GRO-α levels in serum from RA patients treated with infliximab decreased significantly after the initial treatment. The mean RANTES and MIP-1β levels did not change significantly after the treatment. Infliximab treatment significantly lowered the serum GRO-α levels of RA patients. GRO-α is one of the crucial cytokines affected by infliximab treatment. The blocking therapy of RANTES and MIP-1β combined with infliximab treatment may have an additional effect without competition in the TNFα cascade.
- Subjects
RHEUMATOID arthritis; CHEMOKINES; INFLIXIMAB; AUTOIMMUNE diseases; LYMPHOCYTES; CHEMOTAXIS
- Publication
Clinical Rheumatology, 2007, Vol 26, Issue 7, p1088
- ISSN
0770-3198
- Publication type
Article
- DOI
10.1007/s10067-006-0453-5