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. Author manuscript; available in PMC: 2011 Jun 16.
Published in final edited form as: Arthritis Rheum. 2009 Jun;60(6):1604–1614. doi: 10.1002/art.24574

Figure 4.

Figure 4

Tumor necrosis factor α (TNFα) induction by galectin 3 (gal-3) is not the mechanism underlying selective chemokine secretion by synovial fibroblasts. Synovial fibroblasts from patients with rheumatoid arthritis (RA) were seeded and treated with medium (control), recombinant TNFα (10 ng/ml), or recombinant galectin 3 (10 μg/ml). Duplicate wells of cytokine-treated fibroblasts were pretreated with an anti-TNFα blocking antibody. A, Production of interleukin-6 (IL-6), a representative proinflammatory cytokine, after 24 hours of stimulation, as analyzed by enzyme-linked immunosorbent assay (ELISA). B and C, Production of CCL2 (B) and CCL5 (C), representative chemokines, after 24 hours of stimulation, as analyzed by ELISA. Bars show the mean and SD of duplicate assays combined from at least 4 patients. ** = P < 0.01.