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The biological properties of TNF-alpha make it a candidate therapeutic target in RA. Our studies have demonstrated that TNF-alpha and its receptors are up-regulated and co-expressed in the synovium and cartilage-pannus junction of RA joints. Neutralizing TNF-alpha antibodies reduce the production of the many pro-inflammatory cytokines, including IL-1 and granulocyte-macrophage colony-stimulating factor (GM-CSF), produced by mononuclear cells from RA in culture. When injected into DBA/1 mice with collagen-induced arthritis and TNF-alpha transgenic mice with arthritis, anti-TNF MoAbs decrease inflammatory damage of joints. Clinical trials employing cA2, a chimaeric anti-TNF-alpha MoAb, in open-label and randomized placebo-controlled studies have demonstrated a dose-dependent efficacy with impressive improvement in disease activity and acute-phase responses lasting several weeks. We conclude that TNF-alpha is a critical mediator of inflammation in RA, and is an important therapeutic target in this disease.

Original publication

DOI

10.1111/j.1365-2249.1995.tb08340.x

Type

Journal article

Journal

Clinical and experimental immunology

Publication Date

08/1995

Volume

101

Pages

207 - 212

Addresses

Kennedy Institute of Rheumatology, London, UK.

Keywords

Humans, Arthritis, Rheumatoid, Tumor Necrosis Factor-alpha, Antibodies, Monoclonal