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      Update on the challenges and recent advances in cancer immunotherapy

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          Abstract

          This overview provides an analysis of some of the immunotherapies currently in use and under investigation, with a special focus on the tumor microenvironment, which we believe is a major factor responsible for the general failure of immunotherapy to date. It is our expectation that combining immunotherapy with methods of altering the tumor microenvironment and targeting regulatory T cells and myeloid cells will yield favorable results.

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          PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors.

          Michael Curran, Welby Montalvo, Hideo Yagita … (2010)
          Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Flt3-ligand (Fvax) combined with antibody blockade of the negative T-cell costimulatory receptor cytotoxic T-lymphocyte antigen-4 (CTLA-4) promotes rejection of preimplanted tumors. Despite CTLA-4 blockade, T-cell proliferation and cytokine production can be inhibited by the interaction of programmed death-1 (PD-1) with its ligands PD-L1 and PD-L2 or by the interaction of PD-L1 with B7-1. Here, we show that the combination of CTLA-4 and PD-1 blockade is more than twice as effective as either alone in promoting the rejection of B16 melanomas in conjunction with Fvax. Adding alphaPD-L1 to this regimen results in rejection of 65% of preimplanted tumors vs. 10% with CTLA-4 blockade alone. Combination PD-1 and CTLA-4 blockade increases effector T-cell (Teff) infiltration, resulting in highly advantageous Teff-to-regulatory T-cell ratios with the tumor. The fraction of tumor-infiltrating Teffs expressing CTLA-4 and PD-1 increases, reflecting the proliferation and accumulation of cells that would otherwise be anergized. Combination blockade also synergistically increases Teff-to-myeloid-derived suppressor cell ratios within B16 melanomas. IFN-gamma production increases in both the tumor and vaccine draining lymph nodes, as does the frequency of IFN-gamma/TNF-alpha double-producing CD8(+) T cells within the tumor. These results suggest that combination blockade of the PD-1/PD-L1- and CTLA-4-negative costimulatory pathways allows tumor-specific T cells that would otherwise be inactivated to continue to expand and carry out effector functions, thereby shifting the tumor microenvironment from suppressive to inflammatory.
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            Cancer immunotherapy: moving beyond current vaccines.

            Steven Rosenberg, James Yang, Nicholas Restifo (2004)
            Great progress has been made in the field of tumor immunology in the past decade, but optimism about the clinical application of currently available cancer vaccine approaches is based more on surrogate endpoints than on clinical tumor regression. In our cancer vaccine trials of 440 patients, the objective response rate was low (2.6%), and comparable to the results obtained by others. We consider here results in cancer vaccine trials and highlight alternate strategies that mediate cancer regression in preclinical and clinical models.
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              Regulatory T cells, tumour immunity and immunotherapy.

              Weiping Zou (2006)
              Tumours express a range of antigens, including self-antigens. Regulatory T cells are crucial for maintaining T-cell tolerance to self-antigens. Regulatory T cells are thought to dampen T-cell immunity to tumour-associated antigens and to be the main obstacle tempering successful immunotherapy and active vaccination. In this Review, I consider the nature and characteristics of regulatory T cells in the tumour microenvironment and their potential multiple suppressive mechanisms. Strategies for therapeutic targeting of regulatory T cells and the effect of regulatory T cells on current immunotherapeutic and vaccine regimens are discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Immunotargets Ther
                Journal ID (iso-abbrev): Immunotargets Ther
                Journal ID (publisher-id): ImmunoTargets and Therapy
                Title: ImmunoTargets and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 2253-1556
                Publication date Collection: 2013
                Publication date (Electronic): 15 June 2013
                Volume: 2
                Pages: 39-49
                Affiliations
                [1 ]Centro Medico Demetra: Hyperthermia and Immunity Center, Terni, Italy
                [2 ]Integrated Health Clinic, Fort Langley, British Columbia, Canada
                [3 ]Blokhin Cancer Research Center, Russian Academy of Medical Sciences, Moscow, Russia
                Author notes
                Correspondence: Gianfranco Baronzio, Centro Medico Demetra: Hyperthermia and Immunity Center, via Cassian Bon, 1/A 05100 Terni, Italy, Tel +39 331 877 872, Email barongf@ 123456intercom.it
                Article
                Publisher ID: itt-2-039
                DOI: 10.2147/ITT.S30818
                PMC ID: 4928368
                PubMed ID: 27471687
                SO-VID: e6d2c9c1-d53d-427a-afc2-f376e334ed23
                Copyright © © 2013 Baronzio et al, publisher and licensee Dove Medical Press Ltd
                License:

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                Categories
                Subject: Review

                Keywords: tumor microenvironment,tumor immunity,immunosuppression,ctla-4,pd-1,exosomes,myeloid-derived suppressor cells,tregs
                Data availability:
                Keywords: tumor microenvironment, tumor immunity, immunosuppression, ctla-4, pd-1, exosomes, myeloid-derived suppressor cells, tregs

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