Influence of immunogenicity on the long-term efficacy of infliximab in Crohn's disease.
By F. Baert, M. Noman, Severine Vermeire, G. Van Assche, G. D' Haens, A. Carbonez, P. Rutgeerts. New England Journal of Medicine, 2003
2,082 citations recorded by the source corpus.
Subfields: Genetics, Immunology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/85abcf691f597cb4ab2b1514c90ed558c4f1c84d
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Citations in the corpus
- TNF and TNF-receptors: From mediators of cell death and inflammation to therapeutic giants - past, present and future. (2014, background): “This was initially thought to be more likely for anti-TNF antibodies that contain murine Ig components such as IFX [224], but neutralizing and immune complex forming anti-drug antibodies can also arise during treatment with fully humanized mAbs such as ADA [225].”
- Trough concentrations of infliximab guide dosing for patients with inflammatory bowel disease. (2015, methodology): “Based on a previously reported clinically relevant cut-off for ATI, we chose to exclude 6 patients with high ATI and to discontinue their infliximab, as ATI are associated with impaired response to treatment and serious adverse events, such as acute infusion reactions.(7) Therapeutic drug”
- Guidelines for the management of inflammatory bowel disease in adults (2011, background): “Antibodies to infliximab (ATI) can trigger both acute infusion reactions and delayed serum-sickness-like reactions. Minor acute reactions usually respond to slowing the infusion rate or treatment with antihistamines, paracetamol and sometimes corticosteroids. Anti-histamines and steroids can be used”
- Therapeutic antibodies for autoimmunity and inflammation (2010, background): “Patients with Crohn's disease treated with infliximab develop human anti-chimeric antibodies (HACAs) in 8–61% of patient”
- Tumor necrosis factor antagonist mechanisms of action: a comprehensive review. (2008, background): “Although each of the tested agents bound to a tmTNF-transfected human cell line, infliximab and adalimumab were somewhat more active than etanercept in mediating CDC and ADCC, and certolizumab was inactive, as would be expected for an Fab' molecule (Fossati & Nesbitt, 2005a; Gramlick et al., 2006).”