Abstract
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 cytotoxicity (ADCC) was demonstrated in RSCL. In contrast, in vitro exposure of RRCL to alemtuzumab resulted in a significant degree of CMC and ADCC. Of note, in vitro blocking of CD52 with anti-CD52 F(ab')(2) fractions in RRCL improved rituximab-associated CMC as compared to unblocked RRCL. Our current data provides a basis for further evaluation of alemtuzumab-based clinical trials for patients with rituximab-resistant NHL.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Alemtuzumab
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Antibodies, Monoclonal / immunology
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Antibodies, Monoclonal / therapeutic use*
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Antibodies, Monoclonal, Humanized
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Antibodies, Monoclonal, Murine-Derived
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Antibodies, Neoplasm / therapeutic use*
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Antibody-Dependent Cell Cytotoxicity*
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Antigens, CD / analysis
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Antigens, CD20 / analysis
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Antigens, Neoplasm / analysis
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Antineoplastic Agents / therapeutic use*
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Apoptosis
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CD52 Antigen
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Cell Line, Tumor
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Complement System Proteins / immunology*
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Cytotoxicity, Immunologic
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Drug Resistance, Neoplasm
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Glycoproteins / analysis
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Glycoproteins / antagonists & inhibitors*
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Histocompatibility Antigens Class II / analysis
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Humans
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Lymphoma, Non-Hodgkin / drug therapy*
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Lymphoma, Non-Hodgkin / immunology
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Rituximab
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antibodies, Monoclonal, Murine-Derived
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Antibodies, Neoplasm
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Antigens, CD
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Antigens, CD20
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Antigens, Neoplasm
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Antineoplastic Agents
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CD52 Antigen
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CD52 protein, human
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Glycoproteins
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Histocompatibility Antigens Class II
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Alemtuzumab
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Rituximab
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Complement System Proteins