Tumor necrosis factor and granuloma biology: explaining the differential infection risk of etanercept and infliximab.
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.
Wallis
Robert S
RS
UMDNJ-New Jersey Medical School, Newark, NJ, USA. robert.wallis@columbia.ppdi.com
Ehlers
Stefan
S
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000037:antagonists & inhibitors*; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D000068800:Etanercept; D006099:Granuloma / Q000139:chemically induced*; D006801:Humans; D007074:Immunoglobulin G; D007239:Infections / Q000139:chemically induced*; D000069285:Infliximab; D018124:Receptors, Tumor Necrosis Factor / Q000037:antagonists & inhibitors*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept