Journal
TRENDS IN IMMUNOLOGY
Volume 25, Issue 3, Pages 158-164Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2004.01.008
Keywords
-
Categories
Ask authors/readers for more resources
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 beta-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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available