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Letter

The key role of CD40 ligand in overcoming tumor-induced dendritic cell dysfunction

Alberto Pinzon-Charry1,2 email, Chris W Schmidt1,2 and José Alejandro López1,2 email

Dendritic Cell and Cancer Laboratory, Queensland Institute of Medical Research, Royal Brisbane Hospital Post Office, Brisbane 4019, Australia

School of Medicine, University of Queensland, Herston 4006, Australia

author email corresponding author email

Breast Cancer Research 2006, 8:402doi:10.1186/bcr1386

Published: 22 February 2006


See related commentary by Lenahan and Avigan http://breast-cancer-research.com/content/8/1/101 and related research by Pinzon-Charry et al. http://breast-cancer-research.com/content/8/1/R5 in this issue.

Abstract

Overcoming dendritic cell (DC) dysfunction is a prerequisite for successful active immunotherapy against breast cancer. CD40 ligand (CD40L), a key molecule in the interface between T-lymphocytes and DCs, seems to be instrumental in achieving that goal. Commenting on our data that CD40L protects circulating DCs from apoptosis induced by breast tumor products, Lenahan and Avigan highlighted the potential of CD40L for immunotherapy. We expand on that argument by pointing to additional findings that CD40L not only rescues genuine DCs but also functionally improves populations of immature antigen-presenting cells that fill the DC compartment in patients with breast cancer.


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