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      CD4 and CD8 T lymphocyte interplay in controlling tumor growth

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          Abstract

          The outstanding clinical success of immune checkpoint blockade has revived the interest in underlying mechanisms of the immune system that are capable of eliminating tumors even in advanced stages. In this scenario, CD4 and CD8 T cell responses are part of the cancer immune cycle and both populations significantly influence the clinical outcome. In general, the immune system has evolved several mechanisms to protect the host against cancer. Each of them has to be undermined or evaded during cancer development to enable tumor outgrowth. In this review, we give an overview of T lymphocyte-driven control of tumor growth and discuss the involved tumor-suppressive mechanisms of the immune system, such as senescence surveillance, cancer immunosurveillance, and cancer immunoediting with respect to recent clinical developments of immunotherapies. The main focus is on the currently existing knowledge about the CD4 and CD8 T lymphocyte interplay that mediates the control of tumor growth.

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          Pan-cancer Immunogenomic Analyses Reveal Genotype-Immunophenotype Relationships and Predictors of Response to Checkpoint Blockade.

          Pornpimol Charoentong, Francesca Finotello, Mihaela Angelova … (2017)
          The Cancer Genome Atlas revealed the genomic landscapes of human cancers. In parallel, immunotherapy is transforming the treatment of advanced cancers. Unfortunately, the majority of patients do not respond to immunotherapy, making the identification of predictive markers and the mechanisms of resistance an area of intense research. To increase our understanding of tumor-immune cell interactions, we characterized the intratumoral immune landscapes and the cancer antigenomes from 20 solid cancers and created The Cancer Immunome Atlas (https://tcia.at/). Cellular characterization of the immune infiltrates showed that tumor genotypes determine immunophenotypes and tumor escape mechanisms. Using machine learning, we identified determinants of tumor immunogenicity and developed a scoring scheme for the quantification termed immunophenoscore. The immunophenoscore was a superior predictor of response to anti-cytotoxic T lymphocyte antigen-4 (CTLA-4) and anti-programmed cell death protein 1 (anti-PD-1) antibodies in two independent validation cohorts. Our findings and this resource may help inform cancer immunotherapy and facilitate the development of precision immuno-oncology.
          Article 0 comments Cited 2291 times – based on 0 reviews     Review now
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            A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17.

            Heon Park, Zhaoxia Li, Xuexian O. Yang … (2005)
            Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-gamma negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
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              IFNgamma and lymphocytes prevent primary tumour development and shape tumour immunogenicity.

              V Shankaran, H. Ikeda, A. T. Bruce … (2001)
              Lymphocytes were originally thought to form the basis of a 'cancer immunosurveillance' process that protects immunocompetent hosts against primary tumour development, but this idea was largely abandoned when no differences in primary tumour development were found between athymic nude mice and syngeneic wild-type mice. However, subsequent observations that nude mice do not completely lack functional T cells and that two components of the immune system-IFNgamma and perforin-help to prevent tumour formation in mice have led to renewed interest in a tumour-suppressor role for the immune response. Here we show that lymphocytes and IFNgamma collaborate to protect against development of carcinogen-induced sarcomas and spontaneous epithelial carcinomas and also to select for tumour cells with reduced immunogenicity. The immune response thus functions as an effective extrinsic tumour-suppressor system. However, this process also leads to the immunoselection of tumour cells that are more capable of surviving in an immunocompetent host, which explains the apparent paradox of tumour formation in immunologically intact individuals.
              Article 0 comments Cited 721 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Norman Woller:
                ORCID: http://orcid.org/0000-0002-4928-0117
                +49 511 532 3732 , woller.norman@mh-hannover.de
                Journal
                Journal ID (nlm-ta): Cell Mol Life Sci
                Journal ID (iso-abbrev): Cell. Mol. Life Sci
                Title: Cellular and Molecular Life Sciences
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1420-682X
                ISSN (Electronic): 1420-9071
                Publication date (Electronic): 14 October 2017
                Publication date PMC-release: 14 October 2017
                Publication date (Print): 2018
                Volume: 75
                Issue: 4
                Pages: 689-713
                Affiliations
                ISNI 0000 0000 9529 9877, GRID grid.10423.34, Clinic for Gastroenterology, Hepatology, and Endocrinology, , Hannover Medical School, ; Carl Neuberg Str. 1, 30625 Hannover, Germany
                Author information
                http://orcid.org/0000-0002-4928-0117
                Article
                Publisher ID: 2686
                DOI: 10.1007/s00018-017-2686-7
                PMC ID: 5769828
                PubMed ID: 29032503
                SO-VID: 8f138939-aef4-4b14-aa46-727ebc73bd42
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 20 June 2017
                Date revision received : 11 October 2017
                Date accepted : 11 October 2017
                Funding
                Funded by: Deutsche Forschungsgemeinschaft
                Award ID: WO 1933/1-2
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer International Publishing AG, part of Springer Nature 2018

                ScienceOpen disciplines: Molecular biology
                Keywords: crosstalk,immunotherapy,immune escape,t cell exhaustion,neoantigen,oncolytic virotherapy,cancer vaccine,immune response,clinical study,cancer mouse model
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: crosstalk, immunotherapy, immune escape, t cell exhaustion, neoantigen, oncolytic virotherapy, cancer vaccine, immune response, clinical study, cancer mouse model

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