Infliximab products neutralize the biological activity of TNF-alpha by binding with high affinity to the soluble and transmembrane forms of TNF-alpha and inhibit binding of TNF-alpha with its receptors. Infliximab products do not neutralize TNF-beta (lymphotoxin-alpha), a related cytokine that utilizes the same receptors as TNF-alpha. Biological activities attributed to TNF-alpha include: induction of pro-inflammatory cytokines such as interleukins (IL) 1 and 6, enhancement of leukocyte migration by increasing endothelial layer permeability and expression of adhesion molecules by endothelial cells and leukocytes, activation of neutrophil and eosinophil functional activity, induction of acute phase reactants and other liver proteins, as well as tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Cells expressing transmembrane TNF-alpha bound by infliximab products can be lysed in vitro or in vivo. Infliximab products inhibit the functional activity of TNF-alpha in a wide variety of in vitro bioassays utilizing human fibroblasts, endothelial cells, neutrophils, B and T-lymphocytes and epithelial cells. The relationship of these biological response markers to the mechanism(s) by which infliximab products exert their clinical effects is unknown. Anti-TNF-alpha antibodies reduce disease activity in the cotton-top tamarin colitis model, and decrease synovitis and joint erosions in a murine model of collagen-induced arthritis. Infliximab products prevent disease in transgenic mice that develop polyarthritis as a result of constitutive expression of human TNF-alpha, and when administered after disease onset, allow eroded joints to heal.