Open AccessDecrease in cellularity and expression of adhesion molecules by anti–tumor necrosis factor α monoclonal antibody treatment in patients with rheumatoid arthritis
Author(s) -
Tak Paul P.,
Taylor Peter C.,
Breedveld Ferdinand C.,
Smeets Tom J. M.,
Daha Mohamed R.,
Kluin Philip M.,
Meinders A. Edo,
Maini Ravinder N.
Publication year - 1996
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780390702
Subject(s) - rheumatoid arthritis , cell adhesion molecule , tumor necrosis factor alpha , medicine , monoclonal antibody , cytokine , adhesion , immunology , cell adhesion , synovial membrane , inflammation , arthritis , necrosis , alpha (finance) , antibody , pathology , chemistry , surgery , organic chemistry , patient satisfaction , construct validity
Objective . The effect of chimeric anti–tumor necrosis factor α (TNFα) monoclonal antibody (MAb) therapy on synovial inflammation was studied in order to address the hypothesis that anti‐TNFα therapy leads to down‐regulation of adhesion molecules and a decrease in inflammatory cell influx in synovial tissue (ST). Methods . The immunohistologic features of synovial biopsy specimens, both before and 4 weeks after anti‐TNFα MAb (cA2) therapy, were studied in 14 patients with rheumatoid arthritis (RA). The patients either received a placebo (n = 2), or were given intravenous doses of cA2 at 10 mg/kg (n = 5) or 20 mg/kg (n = 7). Results . A significant ( P < 0.03) reduction in the mean scores for T cells and for the adhesion molecules, vascular cell adhesion molecule 1 and E‐selectin, was observed after therapy with 10 mg/kg or 20 mg/kg of cA2 in RA patients. Conclusion . The reduced expression of adhesion molecules, and the decrease in cellularity of rheumatoid ST after cA2 administration support the hypothesis the antiinflammatory effect of anti‐TNFα therapy might be partly explained by down‐regulation of cytokine‐inducible vascular adhesion molecules in ST, with a consequent reduction of cell traffic into joints.