PuSH - Publication Server of Helmholtz Zentrum München: Rituximab and Alemtuzumab induce a nonclassic, caspase-independent apoptotic pathway in B-lymphoid cell lines and in chronic lymphocytic leukemia cells.

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Stanglmaier, M. ; Reis, S. ; Hallek, M.

Rituximab and Alemtuzumab induce a nonclassic, caspase-independent apoptotic pathway in B-lymphoid cell lines and in chronic lymphocytic leukemia cells.

Ann. Hematol. 83, 634-645 (2004)

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Open Access Green as soon as Postprint is submitted to ZB.

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The monoclonal antibodies (MoAbs) alemtuzumab (anti-CD52) and rituximab (anti-CD20) produce objective clinical responses in patients with chronic lymphocytic leukemia (CLL). However, their mechanisms of action are not fully understood. Therefore, we investigated the mechanisms of lymphoma and CLL cell killing by two anti-CD20 antibodies (rituximab, B1) and by alemtuzumab. All antibodies induced complement-independent cell death in B-lymphoid cell lines Raji, Ramos, and Mec-1. The efficiency of cell killing was increased by the addition of human complement in Raji but not Ramos cells. Both alemtuzumab and rituximab also killed freshly isolated CLL cells, with a much stronger response for alemtuzumab (from eight of eight patients) compared to rituximab (from two of six patients). Cell morphology and Western blot analyses revealed that the antibody-induced cell death lacked some typical features of apoptosis such as chromatin condensation or poly-ADP-ribose polymerase (PARP) cleavage. Taken together, the results suggest that the tumor killing activity of these MoAbs is not only mediated by complement-mediated cytotoxicity (CDC) or antibody-dependent cytotoxicity (ADCC), but also by a nonclassic, caspase-independent apoptotic pathway.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords chronic lymphocytic leukemia; monoclonal antibody therapy; CD20; CD52; caspase-independent apoptosis

ISSN (print) / ISBN 0939-5555

e-ISSN 1432-0584

Journal Annals of Hematology

Quellenangaben Volume: 83, Issue: 10, Pages: 634-645

Publisher Springer

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Molecular Immunology (IMI)