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

Abstract

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.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2013
Accession Number
ADA585489

Entities

People

  • M. E. Medof

Organizations

  • Case Western Reserve University

Tags

DTIC Thesaurus Topics

  • Angiogenesis
  • Biological Factors
  • Biomedical Research
  • Blood
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Endothelial Cells
  • Growth Factors
  • Lymphocytes
  • Neoplasms
  • Peptide Growth Factors
  • Peptides
  • Production
  • Proteins

Fields of Study

  • Biology
  • Medicine

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology
  • Trauma Surgery or Emergency Medicine.