Detection of tumor necrosis factor α but not tumor necrosis factor β in rheumatoid arthritis synovial fluid and serum

Abstract

Synovial fluids from 6 of 12 patients with rheumatoid arthritis (RA) and from 3 of 11 patients with reactive arthritis contained measurable levels of tumor necrosis factor α (TNFα). Seven of 12 sera from RA patients contained TNFα, while only 1 of those from reactive arthritis patients was positive. Gamma‐inter‐feron was detected in the synovial fluids and sera of only the RA patients. Tumor necrosis factor β was not detected in any sera or synovial fluids. RA patients with detectable TNFα had higher erythrocyte sedimentation rates and synovial fluid leukocyte counts.

Association of tumor necrosis factor α polymorphism, but not the shared epitope, with increased radiographic progression in a seropositive rheumatoid arthritis inception cohort

“…Vinasco et al (57) found more frequent nodular disease in their cohort of adult RA patients with the TNFA -308 AA plus AG genotypes. High levels of TNF␣ are associated with more severe disease in RA (58), and elevated levels of TNF␣ are found in the synovial fluid and synovial tissue of RA patients (25). These published findings and our findings of increased radiographic progression suggest that the -308 polymorphism may have functional significance by increasing the production of TNF␣.…”

“…RA is associated with cytokine network dysfunction (23), particularly TNF␣, which mediates a broad range of proinflammatory and immunostimulatory activities (24). Elevated levels of TNF␣ are found in the synovial fluid and synovial tissue of RA patients (25).…”

Enhanced Production Of Interleukin‐1 And Tumor Necrosis Factor α By Cultured Peripheral Blood Monocytes From Patients With Scleroderma

“…Saxne et al reported the detection of TNFa in synovial fluids and sera from some of their patients with rheumatoid arthritis (13). but neither TNFa production nor TNFa activity has been shown in patients with SSc.…”

Electro-gene therapy of collagen-induced arthritis by using an expression plasmid for the soluble p75 tumor necrosis factor receptor-Fc fusion protein

“…1 Although the causes of RA are not fully understood, various experimental and clinical studies suggest that proinflammatory cytokines, particularly tumor necrosis factor-a (TNF-a), play an important role in RA pathogenesis. [2][3][4][5][6] TNF concentrations are increased in the synovial fluid of persons with active RA 7,8 and increased plasma levels of TNF are associated with joint pain. 9 There are two distinct type cell-surface TNF receptors (TNFRs), designated p55 and p75.…”