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

被引：110

作者：

Wallis, RS

Ehlers, S

机构：

[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA

[2] PPD Dev, Columbia, MD USA

[3] Leibniz Ctr Med & Biosci, Res Ctr Borstel, D-23845 Borstel, Germany

来源：

SEMINARS IN ARTHRITIS AND RHEUMATISM | 2005年 / 34卷 / 05期

关键词：

D O I：

10.1016/j.semarthrit.2005.01.009

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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. (c) 2005 Elsevier Inc. All rights reserved.

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页码：34 / 38

页数：5

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