Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis.
By J. Golay, L. Zaffaroni, T. Vaccari, M. Lazzari, G. Borleri, S. Bernasconi, Francesco Saverio Tedesco, A. Rambaldi, M. Introna. Blood, 2000
677 citations recorded by the source corpus.
Subfields: Immunology, Pathology and Forensic Medicine, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/e1f9a2957e35ba4f9a9c1ab584ddf41f7498ec54
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Citations in the corpus
- Non-commercial Research and Educational Use including without Limitation Use in Instruction at Your Institution, Sending It to Specific Colleagues That You Know, and Providing a Copy to Your Institution's Administrator. All Other Uses, Reproduction and Distribution, including without Limitation Comm (2005, neutral): “The value of a small number of bits is changed randomly by a mutation operator.”
- Rituximab (monoclonal anti-CD20 antibody): mechanisms of action and resistance (2003, background): “A recent report suggests, based on data with nonsaturating levels of anti-CD20, that an overall assessment of the levels of both CD20 and the complement inhibitory proteins can predict in vitro sensitivity to rituximab-mediated CDC, and that this may correlate with clinical response (Manches et al.,”
- Early results of a chemoimmunotherapy regimen of fludarabine, cyclophosphamide, and rituximab as initial therapy for chronic lymphocytic leukemia. (2005, background): “In some cell lines, fludarabine exposure results in downregulation of the complementdefense proteins CD55 and CD59.(18,19) Clinical trials in low-grade and intermediate-grade lymphoma strongly suggest higher response rates and even longer survival when rituximab is added to chemotherapy regimens.”
- Complement Activation Determines the Therapeutic Activity of Rituximab In Vivo 1 (2003, methodology): “Although less efficiently, rituximab also activates Ab-dependent cellular cytotoxicity (ADCC) in vitro (3, 8), and recent evidence showing a correlation between Fc RIII polymorphisms and clinical response suggests a role for Fc RIIIbearing cells such as NK cells and macrophages in the response (12).”