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Clinical and Developmental Immunology
Volume 2011, Article ID 609579, 12 pages
Review Article

Toll-Like Receptor 4 Activation in Cancer Progression and Therapy

Alja Oblak1,2 and Roman Jerala1,2,3

1Department of Biotechnology, National Institute of Chemistry, 1000 Ljubljana, Slovenia
2EN-FIST Centre of Excellence, 1000 Ljubljana, Slovenia
3Faculty of Chemistry and Chemical Technology, University of Ljubljana, 1000 Ljubljana, Slovenia

Received 1 July 2011; Accepted 1 September 2011

Academic Editor: David Kaplan

Copyright © 2011 Alja Oblak and Roman Jerala. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cancer immunotherapy has been the focus of intense research since the late 19th century when Coley observed that bacterial components can contribute to cancer regression by eliciting an antitumor immune response. Successful activation and maturation of tumor-specific immune cells is now known to be mediated by bacterial endotoxin, which activates Toll-like receptor 4 (TLR4). TLR4 is expressed on a variety of immune as well as tumor cells, but its activation can have opposing effects. While TLR4 activation can promote antitumor immunity, it can also result in increased tumor growth and immunosuppression. Nevertheless, TLR4 engagement by endotoxin as well as by endogenous ligands represents notable contribution to the outcome of different cancer treatments, such as radiation or chemotherapy. Further research of the role and mechanisms of TLR4 activation in cancer may provide novel antitumor vaccine adjuvants as well as TLR4 inhibitors that could prevent inflammation-induced carcinogenesis.