Box 1. Activation and regulation of the complement system

Complement activation by mAbs can cause direct tumor cell lysis or enhance antibody-dependent cell-mediated cytotoxicity. However, tumor cells are protected from complement-mediated injury by membrane-bound complement regulatory proteins (mCRP) that are often expressed at elevated levels on tumor ce...

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Bibliographic Details
Published in:Trends in immunology 2004-03, Vol.25 (3), p.158
Main Authors: Gelderman, Kyra A, Tomlinson, Stephen, Ross, Gordon D, Gorter, Arko
Format: Article
Language:English
Subjects:
Binding sites
Breast cancer
Cancer therapies
Clinical trials
Colorectal cancer
Cytotoxicity
Hematology
Immunotherapy
Leukemia
Lung cancer
Lymphoma
Microorganisms
Tumors
Yeast
Online Access:Get full text
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Summary:Complement activation by mAbs can cause direct tumor cell lysis or enhance antibody-dependent cell-mediated cytotoxicity. However, tumor cells are protected from complement-mediated injury by membrane-bound complement regulatory proteins (mCRP) that are often expressed at elevated levels on tumor cells. Recent studies indicate that blocking or overwhelming the function of tumor cell mCRP might substantially improve the efficacy of monoclonal antibody (mAb) immunotherapy. In addition, the use of β-glucan as an adjuvant for mAb immunotherapy enables iC3b deposited on tumor cells by mAbs to activate complement receptor 3 (CR3) on effector cells, thus inducing CR3-dependent cellular cytotoxicity. These strategies provide novel cell-mediated mechanisms of tumor cytotoxicity that are additive to all other mAb effector mechanisms.
ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2004.01.008