Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn's disease.
By Jan M. H. Van den Brande, H. Braat, G. R. van den Brink, H. Versteeg, C. A. Bauer, Inge Hoedemaeker, C. van Montfrans, D. Hommes, M. Peppelenbosch, S. V. van Deventer. Gastroenterology, 2003
756 citations recorded by the source corpus.
Subfields: Genetics, Rheumatology
View Paper: https://www.semanticscholar.org/paper/0fa72866693a433cffe272feca726c2b7b51b6d5
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Citations in the corpus
- Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: systematic review and meta-analysis of rare harmful effects in randomized controlled trials. (2006, background): “But unlike etanercept, anti-TNF antibodies also induce apoptosis in highly activated lymphocytes from patients with Crohn disease.(48) In addition, the antibodies have a more potent effect on lipoprotein serine–induced cytokine release in macrophages compared with etanercept.”
- Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. (2008, background): “…Brande et al., 2003), a TNF-transfected Jurkat human T-cell line (Mitoma et al., 2005), lamina propria T cells from patients with Crohn's disease (Van den Brande et al., 2003) or synovial fluid T cells from patients with RA (Catrina et al., 2005), despite demonstrated binding of etanercept to…”
- Therapeutic antibodies for autoimmunity and inflammation (2010, background): “A proposed mechanism by which infliximab, and not etanercept, was thought to be efficacious in Crohn's disease was the ability of infliximab to bind membrane-associated TNF and induce apoptosis of activated T cells and macrophage”
- TNF and TNF-receptors: From mediators of cell death and inflammation to therapeutic giants - past, present and future. (2014, background): “activation-induced cell death [207,208], or that anti-TNF antibodies inhibit T cell proliferation and cytokine secretion and induce regulatory macrophages via FcR interactions [209].”