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      Enhanced tumor eradication by combining CTLA-4 or PD-1 blockade with CpG therapy.

      Journal of Immunotherapy (Hagerstown, Md. : 1997)
      Animals, Antibodies, administration & dosage, immunology, Antigens, CD, Antigens, Surface, genetics, metabolism, Antineoplastic Combined Chemotherapy Protocols, therapeutic use, Apoptosis Regulatory Proteins, BCG Vaccine, CD4-Positive T-Lymphocytes, drug effects, CD8-Positive T-Lymphocytes, CTLA-4 Antigen, Cell Line, Tumor, Female, Flow Cytometry, Gene Expression Regulation, Neoplastic, Lysosomal-Associated Membrane Protein 1, Mice, Mice, Inbred C57BL, Oligodeoxyribonucleotides, Programmed Cell Death 1 Receptor, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, Regulatory, Transforming Growth Factor beta, Treatment Outcome, Tumor Burden, Urinary Bladder Neoplasms, drug therapy, pathology

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          Abstract

          Tumor immunotherapy aims to break effector T-cell anergy and to block suppressive cell types and ligands allowing effector cells to exert tumor eradication. Previous reports demonstrate that cytotoxic T lymphocyte antigen-4 (CTLA-4)-blocking antibodies promote T-cell activation and render T effector cells resistant to T regulatory cells (Tregs) whereas programmed death receptor-1 (PD-1)/PD-L1 blockade results in loss of peripheral tolerance. Herein, we explored single or combined antibody blockade of CTLA-4 and PD-1 alone or combined with the toll-like receptor agonists CpG or bacillus Calmette-Guérin for treatment of murine experimental bladder cancer. In therapeutic studies, tumors were rejected by anti-CTLA-4 (aCTLA-4) while anti-PD-1 (aPD-1) suppressed tumor growth. The combination had no additive effect compared with aCTLA-4 alone. However, elevated levels of circulating CD107a expressing CD8 T cells were found in the aCTLA-4 plus aPD-1 group. In addition, levels of antinuclear antibodies correlated inversely with tumor size. Next, we combined CpG or bacillus Calmette-Guérin with aCTLA-4, aPD-1, or aPD-L1 and found that CpG in combination with aCTLA-4 or aPD-1 increased the survival of mice, with aPD-1 plus CpG being superior to either agent alone. CpG plus aCTLA-4 or aPD-1 increased the numbers of circulating tumor-specific CD107a expressing CD8 T cells as well as activated (CD25FoxP3-) CD4 splenocytes. Further, we investigated the numbers of Tregs in the tumor area of treated animals and detected decreased levels after aCTLA-4 or aPD-1 plus CpG therapy. Thus, the combination of CpG with CTLA-4 or PD-1 blockade improved long-term survival and led to increased levels of tumor-reactive T cells and reduced numbers of Tregs at the tumor site.

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