Augmentation of Antitumor T-Cell Responses by Increasing APC T-Cell C5a/C3a-C5aR/C3aR Interactions.

摘要

While we initially found that T effector cell responses against breast cancers can be augmented by increasing C3a and C5a receptor (C3aR/C5aR) signaling by antigen presenting dendritic cell dendritic (DCs) by blocking the function of decay accelerating factor (DAF), we have found that in breast cancers themselves and vascular endothelial cells C3aR/C5aR signaling promotes breast cancer growth. In the past years, we have found that blockade of C3aR/C5aR signaling in CD4+ cells enables endogenous TGF-b1 production and Foxp3 T regulatory cells induction. We are developing ways to control these effects and have prepared specialized mice for testing the clinical efficacy of our findings.