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      Role of Immune Escape Mechanisms in Hodgkin's Lymphoma Development and Progression: A Whole New World with Therapeutic Implications

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          Abstract

          Hodgkin's lymphoma represents one of the most frequent lymphoproliferative syndromes, especially in young population. Although HL is considered one of the most curable tumors, a sizeable fraction of patients recur after successful upfront treatment or, less commonly, are primarily resistant. This work tries to summarize the data on clinical, histological, pathological, and biological factors in HL, with special emphasis on the improvement of prognosis and their impact on therapeutical strategies. The recent advances in our understanding of HL biology and immunology show that infiltrated immune cells and cytokines in the tumoral microenvironment may play different functions that seem tightly related with clinical outcomes. Strategies aimed at interfering with the crosstalk between tumoral Reed-Sternberg cells and their cellular partners have been taken into account in the development of new immunotherapies that target different cell components of HL microenvironment. This new knowledge will probably translate into a change in the antineoplastic treatments in HL in the next future and hopefully will increase the curability rates of this disease.

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          Most cited references244

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          Myeloid-derived suppressor cells: linking inflammation and cancer.

          Suzanne Ostrand-Rosenberg, Pratima Sinha (2009)
          Many cancer immunotherapies developed in experimental animals have been tested in clinical trials. Although some have shown modest clinical effects, most have not been effective. Recent studies have identified myeloid-origin cells that are potent suppressors of tumor immunity and therefore a significant impediment to cancer immunotherapy. "Myeloid-derived suppressor cells" (MDSC) accumulate in the blood, lymph nodes, and bone marrow and at tumor sites in most patients and experimental animals with cancer and inhibit both adaptive and innate immunity. MDSC are induced by tumor-secreted and host-secreted factors, many of which are proinflammatory molecules. The induction of MDSC by proinflammatory mediators led to the hypothesis that inflammation promotes the accumulation of MDSC that down-regulate immune surveillance and antitumor immunity, thereby facilitating tumor growth. This article reviews the characterization and suppressive mechanisms used by MDSC to block tumor immunity and describes the mechanisms by which inflammation promotes tumor progression through the induction of MDSC.
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            Dynamics of the immune reaction to pancreatic cancer from inception to invasion.

            Carolyn Clark, Sunil R Hingorani, Rosemarie Mick … (2007)
            The dynamics of cancer immunosurveillance remain incompletely understood, hampering efforts to develop immunotherapy of cancer. We evaluated the evolving in vivo immune response to a spontaneous tumor in a genetically defined mouse model of pancreatic ductal adenocarcinoma from the inception of preinvasive disease to invasive cancer. We observed a prominent leukocytic infiltration even around the lowest grade preinvasive lesions, but immunosuppressive cells, including tumor-associated macrophages, myeloid-derived suppressor cells (MDSC), and regulatory T cells (Treg), dominated the early response and persisted through invasive cancer. Effector T cells, however, were scarce in preinvasive lesions, found in only a subset of advanced cancers, and showed no evidence of activation. The lack of tumor-infiltrating effector T cells strongly correlated with the presence of intratumoral MDSC with a near mutual exclusion. In vitro, we found that MDSC suppressed T-cell proliferation. Overall, our results show that suppressive cells of the host immune system appear early during pancreatic tumorigenesis, preceding and outweighing antitumor cellular immunity, and likely contribute to disease progression. Thus, in contrast to the hypothesis that an early "elimination phase" of cancer immunosurveillance is eventually overwhelmed by a growing invasive tumor, our findings suggest that productive tumor immunity may be undermined from the start. Efforts to test potent inhibitors of MDSC, tumor-associated macrophages, and Treg, particularly early in the disease represent important next steps for developing novel immunotherapy of cancer.
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              Stimulation of CD25(+)CD4(+) regulatory T cells through GITR breaks immunological self-tolerance.

              Jun Shimizu, Sayuri Yamazaki, Takeshi Takahashi … (2002)
              CD25(+)CD4(+) regulatory T cells in normal animals are engaged in the maintenance of immunological self-tolerance. We show here that glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR, also known as TNFRSF18)--a member of the tumor necrosis factor-nerve growth factor (TNF-NGF) receptor gene superfamily--is predominantly expressed on CD25(+)CD4(+) T cells and on CD25(+)CD4(+)CD8(-) thymocytes in normal naïve mice. We found that stimulation of GITR abrogated CD25(+)CD4(+) T cell-mediated suppression. In addition, removal of GITR-expressing T cells or administration of a monoclonal antibody to GITR produced organ-specific autoimmune disease in otherwise normal mice. Thus, GITR plays a key role in dominant immunological self-tolerance maintained by CD25(+)CD4(+) regulatory T cells and could be a suitable molecular target for preventing or treating autoimmune disease.
              Article 0 comments Cited 333 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Dev Immunol
                Journal ID (iso-abbrev): Clin. Dev. Immunol
                Journal ID (publisher-id): CDI
                Title: Clinical and Developmental Immunology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1740-2522
                ISSN (Electronic): 1740-2530
                Publication date (Print): 2012
                Publication date (Electronic): 15 August 2012
                Volume: 2012
                Electronic Location Identifier: 756353
                Affiliations
                1Clinical Oncology Department, Hospital Universitario Virgen Macarena, 41009 Sevilla, Spain
                2Molecular Biology and Research Section, Hospital de Tortosa Verge de la Cinta and IISPV, URV, 43201 Reus, Spain
                3Radiotherapy Department, Hospital Universitario Virgen Macarena, 41009 Sevilla, Spain
                4Clinical Oncology Department, Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain
                5Pathology Department, Hospital de Tortosa Verge de la Cinta and IISPV, URV, 43201 Reus, Spain
                Author notes
                *Luis de la Cruz-Merino: lucme12@ 123456yahoo.es

                Academic Editor: Keith Knutson

                Article
                DOI: 10.1155/2012/756353
                PMC ID: 3426211
                PubMed ID: 22927872
                SO-VID: 864cc65d-ace2-48eb-9ddd-f737b5ba6099
                Copyright © Copyright © 2012 Luis de la Cruz-Merino et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 February 2012
                Date accepted : 5 June 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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