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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / antagonists & inhibitors*
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Antibodies, Monoclonal / adverse effects*
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Etanercept
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Granuloma / chemically induced*
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Humans
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Immunoglobulin G
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Infections / chemically induced*
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Infliximab
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Receptors, Tumor Necrosis Factor / antagonists & inhibitors*
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Tumor Necrosis Factor-alpha / antagonists & inhibitors*
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antibodies, Monoclonal
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Immunoglobulin G
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Receptors, Tumor Necrosis Factor
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Tumor Necrosis Factor-alpha
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Infliximab
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Etanercept