Augmentation of Antitumor T-Cell Responses by Increasing APC T-Cell C5a/C3a-C5aR/C3aR Interactions
Annual rept. 1 Mar 2012-28 Feb 2013
CASE WESTERN RESERVE UNIV CLEVELAND OH
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While we initially found that T effector cell responses against breast cancers can be augmented by increasing C3a and C5a receptor C3aRC5aR 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 C3aRC5aR signaling promotes breast cancer growth. In the past years, we have found that blockade of C3aRC5aR 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.
- Medicine and Medical Research