David P. Carbone, MD, PhD, David R. Gandara, MD, Scott J

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Non–Small-Cell Lung Cancer: Role of the Immune System and Potential for Immunotherapy David P. Carbone, MD, PhD, David R. Gandara, MD, Scott J. Antonia, MD, PhD, Christoph Zielinski, MD, Luis Paz-Ares, MD, PhD Journal of Thoracic Oncology Volume 10, Issue 7, Pages 974-984 (July 2015) DOI: 10.1097/JTO.0000000000000551 Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

FIGURE 1 Adaptive anticancer immunity. The adaptive anticancer immune response is initiated by immature DCs, which capture and process tumor antigens. DCs subsequently undergo maturation and migrate to tumor-draining lymph nodes, where they present tumor antigens within MHC molecules to naïve T cells, triggering a protective T-cell response. T-cell activation requires interaction not only between the antigen–MHC complex on DCs and TCRs but also among an array of co-stimulatory molecules, including CD80/86 on DCs and the CD28 receptor on T cells. The adaptive anticancer immune response culminates with the infiltration of activated cytotoxic T cells into the tumor, killing cancer cells. DC, dendritic cell; MHC, major histocompatibility; TCR, T-cell receptor. Journal of Thoracic Oncology 2015 10, 974-984DOI: (10.1097/JTO.0000000000000551) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

FIGURE 2 Cancer immunoediting. The proposed process of cancer immunoediting consists of three distinct phases: elimination, equilibrium, and escape. In the elimination phase, innate and adaptive immune responses recognize and destroy cancer cells (immunosurveillance), suppressing tumor development. In the equilibrium phase, tumor clones that escape the elimination phase remain dormant, during which tumor growth does not occur but the immunogenicity of the tumor cells continues to be shaped by selective immune pressure. In the escape phase, tumor cell clones that are resistant to the immune system proliferate unchecked. Adapted with permission from Annu Rev Immunol 2011;29:235–271. Journal of Thoracic Oncology 2015 10, 974-984DOI: (10.1097/JTO.0000000000000551) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

FIGURE 3 Immune checkpoints. A, Cytotoxic CTLA-4 is expressed on T cells after activation and competes with the co-stimulatory T-cell CD28 receptor for CD80/86 expressed by APCs, providing an inhibitory signal to the T cell. B, PD-1 receptor is upregulated on activated T cells and subsequently binds to one of its ligands, PD-L1 or PD-L2, which are usually expressed on tumor cells, providing an inhibitory signal to the T cell. APC, antigen-presenting cell; MHC, major histocompatibility; TCR, T-cell receptor; CTLA-4, cytotoxic T-lymphocyte antigen-4; PD-L1/L2, programmed death ligand-1/ligand-2; PD-1, programmed death-1. Adapted with permission from Nat Rev Cancer 2012;12:252–264. Journal of Thoracic Oncology 2015 10, 974-984DOI: (10.1097/JTO.0000000000000551) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions