Cross-priming of cytotoxic T cells promoted by apoptosis-inducing tumor cell reactive antibodies?

J Clin Immunol. 2002 May;22(3):124-30. doi: 10.1023/a:1015463811683.


Humanizing xenogenic monoclonal antibodies (MAbs) by genetic engineering has greatly improved their therapeutic utility and efficacy. The chimeric CD20 MAb C2B8 (Rituximab) is a prominent representative of this new generation of therapeutic MAbs and has been proposed as a treatment of choice for recurrent follicular non-Hodgkin's lymphomas. Treatment of CD20+ B cells with MAb C2B8 triggers several cell-damaging actions including complement-mediated lysis (CDL), antibody-dependent cellular cytotoxicity (ADCC), and MAb-induced induction of apoptosis. We provide an overview of the most prominent mechanisms underlying the efficacy of antibody treatment. We introduce our concept of cross-priming of cytotoxic T-cell responses promoted by apoptosis incucing antibodies. Treatment of tumor cells with antibodies that are capable of inducing a proapoptotic signal via their cell surface target structure may not only contribute to their direct killing but also may induce cellular responses against the tumor, which may have a long-lasting protective effect. We report, using the example of C2B8 anti-CD20 treatment of lymphoma cells, that MAb C2B8-induced apoptosis of lymphoma cells not only kills these cells but also promotes uptake and cross-presentation of lymphoma cell-derived peptides by antigen-presenting dendritic cells (DC), induces maturation of DC, and allows the generation of specific CTL.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antibodies, Heterophile / immunology
  • Antibodies, Heterophile / therapeutic use
  • Antibodies, Neoplasm / immunology*
  • Antibodies, Neoplasm / therapeutic use
  • Apoptosis / immunology*
  • Humans
  • Lymphoma, B-Cell / drug therapy
  • Lymphoma, B-Cell / pathology
  • T-Lymphocytes, Cytotoxic / immunology*


  • Antibodies, Heterophile
  • Antibodies, Neoplasm