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Review
. 2005 Apr;34(5 Suppl1):34-8.
doi: 10.1016/j.semarthrit.2005.01.009.

Tumor necrosis factor and granuloma biology: explaining the differential infection risk of etanercept and infliximab

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Review

Tumor necrosis factor and granuloma biology: explaining the differential infection risk of etanercept and infliximab

Robert S Wallis et al. Semin Arthritis Rheum. 2005 Apr.

Abstract

Several studies show that the risk of granulomatous infections following therapy with the anti-tumor necrosis factor (TNF) antibody infliximab is higher than after treatment with the soluble TNFRp75 immunoglobulin fusion construct etanercept. Therefore, despite sharing a common target, it is possible that the actual mode of action of the 2 biologicals differs in vivo. TNF is known to participate in the induction and maintenance of protective granulomas at multiple steps, and evidence supporting a differential inhibition of TNF bioactivity and signaling by the 2 drugs is discussed.

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