CD52 over-expression affects rituximab-associated complement-mediated cytotoxicity but not antibody-dependent cellular cytotoxicity: preclinical evidence that targeting CD52 with alemtuzumab may reverse acquired resistance to rituximab in non-Hodgkin lymphoma.

@article{Cruz2007CD52OA,
  title={CD52 over-expression affects rituximab-associated complement-mediated cytotoxicity but not antibody-dependent cellular cytotoxicity: preclinical evidence that targeting CD52 with alemtuzumab may reverse acquired resistance to rituximab in non-Hodgkin lymphoma.},
  author={Raymond I Cruz and Francisco J Hernandez-Ilizaliturri and Scott H Olejniczak and George Michael Deeb and Joy Knight and Paul Wallace and Beth L. Thurberg and William Kennedy and Myron S. Czuczman},
  journal={Leukemia & lymphoma},
  year={2007},
  volume={48 12},
  pages={2424-36}
}
In an attempt to define mechanisms by which B-cell non-Hodgkin lymphoma (NHL) may escape rituximab immunotherapy, we developed several rituximab-resistant cell lines (RRCL) generated from the rituximab-sensitive cell lines (RSCL) Raji and RL. Rituximab resistance was associated with CD20 downregulation and upregulation of CD52 and the complement inhibitory proteins (CIPs) CD55 and CD59. No significant alemtuzumab-associated complement-mediated cell lysis (CMC) or antibody-dependent cellular… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 18 extracted citations

Novel antibody therapy in acute lymphoblastic leukemia.

Current hematologic malignancy reports • 2014
View 1 Excerpt

Complement activation by (auto-) antibodies.

Molecular immunology • 2011
View 1 Excerpt

Similar Papers

Loading similar papers…