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Review
. 2016 Sep 29;35(1):157.
doi: 10.1186/s13046-016-0439-3.

Trends and advances in tumor immunology and lung cancer immunotherapy

Mohanad Aldarouish  1 , Cailian Wang  2
Affiliations
Review

Trends and advances in tumor immunology and lung cancer immunotherapy

Mohanad Aldarouish et al. J Exp Clin Cancer Res. .

Abstract

Among several types of tumor, lung cancer is considered one of the most fatal and still the main cause of cancer-related deaths. Although chemotherapeutic agents can improve survival and quality of life compared with symptomatic treatment, cancers usually still progress after chemotherapy and are often aggravated by serious side effects. In the last few years there has been a growing interest in immunotherapy for lung cancer based on promising preliminary results in achieving meaningful and durable treatments responses with minimal manageable toxicity. This article is divided into two parts, the first part discusses the role of human immune system in controlling and eradicating cancer and the mechanisms of immune response evasion by tumor. The second part reviews the recent progress made in immunotherapy for lung cancer with results from trials evaluating therapeutic vaccines in addition to immune checkpoint blockade, specifically cytotoxic T lymphocyte associated protein 4, programmed death receptor 1 pathway, using monoclonal antibodies.

Keywords: Cancer vaccines; Clinical trials; Immune checkpoint inhibitors; Immunotherapy; Lung cancer; Tumor immunology.

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Figures

Fig. 1
Fig. 1
A schematic representation of the role of innate immune cell subsets in tumor immunity. Blue arrows represent the anti-tumor action, Red arrows represent the inhibition of anti-tumor immunity. TAM: Tumor Associated Macrophages, M1: Classically Activated Macrophages, M2: Alternatively Activated Macrophages, NK: Natural Killer cells, CTL: Cytotoxic Lymphocytes, VEGF: Vascular Endothelial Growth Factor, GM-CSF: Granulocyte-Macrophage Colony-Stimulating Factor, M-CSF: Macrophage Colony-Stimulating Factor, TGF-β: Transforming Growth Factor-Beta, Ab: Antibody. Note: T and B cells are related to the adaptive immune response
Fig. 2
Fig. 2
A schematic representation of the role of adaptive immune cell subsets in tumor immunity. Blue arrows represent the anti-tumor action, Red arrows represent the inhibition of anti-tumor immunity. TNF-α: Tumor necrosis factor alpha, IFN-ɣ: Interferon gamma, CTLs: CD8+ cytotoxic lymphocytes, TGF-β: Transforming growth factor beta, MDSC: Myeloid-derived suppressor cells
Fig. 3
Fig. 3
T cell activation and inactivation mechanism. a upon infection the full activation of specific T cell immune response requires two signals; binding of MHC/Ag complex on the APC (ex: DC) with T cell receptor (TCR) and interaction of B7-molecules (CD80/86) to their ligand (CD28) on the surface of T cell. b Activated T cell expresses a surface immunosuppressive molecule called CTLA-4 which compete with CD28 molecule to bind the B7 molecules. The balance between activation and inactivation signals keeps cytotoxic activity in check, while allowing T-cell function to work in a self-limited manner. c Tumor cells produce a suppressive cytokine that lead to the upregulation of CTLA-4 on the surface of T cells. This mechanism allows tumor cells to evade the cytotoxic effect of T cells
Fig. 4
Fig. 4
The mechanism of PD-1/PD-L1 pathway. Programmed cell death-1 (PD-1) receptor is expressed on the surface of activated T cells, B cells, monocytes, NK cells, and many TILs. Its ligand, PD-L1 is expressed on the surface of resting T cells, B cells, dendritic cells, macrophages, vascular endothelial cells, and pancreatic islet cells. The binding between PD-1 and PD-L1 leads to transmitting of an inhibitory signal into the T cell which reduces cytokine production and suppresses T-cell proliferation. PDL-1 is over expressed on tumor cells by which PD-1/PD-L1 interaction inhibits the proliferation, survival, and effector function of CTL and thus induces apoptosis of tumor-infiltrating T cells
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