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NK cell-mediated lysis is essential to kill Epstein-Barr virus transformed lymphoblastoid B cells when using rituximab. | LitMetric

NK cell-mediated lysis is essential to kill Epstein-Barr virus transformed lymphoblastoid B cells when using rituximab.

Biomed Pharmacother

Department of Microbiology, Tumor and Cell Biology (MTC) and Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institute, Stockholm, Sweden.

Published: July 2009

AI Article Synopsis

  • Rituximab is a monoclonal antibody that targets CD20 and is used to treat various B cell lymphomas and immune disorders like posttransplant lymphoproliferative disorder (PTLD), with a response rate of 65%.
  • Although its exact mechanism is unclear, suggested processes include antibody-dependent cell-mediated cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and inducing cell death directly.
  • Research showed that rituximab alone did not effectively kill EBV-transformed B cells but was successful in promoting CDC and ADCC, particularly when combined with fresh human plasma, indicating that monitoring complement levels and NK cell activity may improve treatment predictions and outcomes for PTLD patients.

Article Abstract

Rituximab is a humanized chimeric monoclonal antibody, targeted against the pan B cell marker CD20. It is frequently used to treat a variety of B cell lymphomas and immunosuppression associated lymphoproliferations such as posttransplant lymphoproliferative disorder (PTLD). The response rate of rituximab treatment is 65%, but the exact in vivo mechanism of action is not yet fully understood, although antibody-dependent cell-mediated cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis have been suggested as effector mechanism. Rituximab may affect different types of lymphomas through different mechanisms. As lymphoblastoid cell lines (LCLs) are well-established in vitro models of PTLD, we investigated the effect of rituximab on these cells using a custom built automated laser confocal fluorescent microscope. We found that rituximab alone was not effective at inducing cell death of EBV-transformed B cells. The antibody was effective in the complement-mediated CDC. Rituximab could induce NK cell-mediated ADCC but it was more effective in the presence of untreated fresh human plasma compared to heat-inactivated human plasma. Our data suggest that complement-enhanced NK-mediated ADCC is required for effective rituximab mediated killing of EBV-transformed B cells. Determining and monitoring of serum complement levels and in vitro killing efficacy of NK cells of PTLD patients might help to predict resistant cases to rituximab therapy. On the other hand our results suggest a possibility that rituximab should be combined only with cytotoxic drugs that spare NK function when treating PTLD patients.

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Source
http://dx.doi.org/10.1016/j.biopha.2008.08.009DOI Listing

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