Harnessing the immune response to treat cancer

Abstract

It is well established that the immune system has the capacity to attack malignant cells. During malignant transformation cells acquire numerous molecular and biochemical changes that render them potentially vulnerable to immune cells. Yet it is self-evident that a growing tumour has managed to evade these host defence mechanisms. The exact ways in which the immune system interacts with tumour cells and how cancers are able to escape immunological eradication have only recently started to be fully elucidated. Understanding the relationship between the tumour and the anti-tumour immune response and how this can be altered with conventional treatments and immune-targeted therapies is crucial to developing new treatments for patients with cancer. In this review, focusing on the anti-tumour T-cell response, we summarize our understanding of how tumours, cancer treatments and the immune system interact, how tumours evade the immune response and how this process could be manipulated for the benefit of patients with cancer.

Chemokines in tumor development and progression

“…CXCL5 and CXCL12 also induce MDSC infiltration in mouse mammary adenocarcinoma [51] (Figure 2). However, the roles of chemokines in MDSC recruitment in human are still poorly Anti-tumor responses are attributable to several types of cells infiltrating into a tumor site, such as tumor infiltrating lymphocytes (TIL) and dendritic cells [54].…”

Harnessing the Immune System to Fight Cancer: The Promise of Genetic Cancer Vaccines

“…In analyzing vaccine delivery systems a greater attention will be given to genetic vaccines which we believe represent the most promising methods to elicit immune responses against a wide variety of tumour antigens especially when administered in combined immunization protocols (heterologous prime/boost). We invite the reader to other recent excellent reviews for aspects of tumour immunology and cancer immunotherapy that we may have missed in our work (Steer et al, 2010;Klebanoff et al, 2011;Palucka et al, 2011;Vergati et al, 2010;Aldrich et al, 2010) .…”

Infiltrating CTLs are bothered by HLA-E on tumors

“…In recent years, focus shifted to the identification of mechanisms responsible for the magnitude and efficacy of antitumor immune responses, such as FoxP3 + regulatory T lymphocytes (Treg), and downregulation of classical Major Histocompatibility Complex (MHC) class I molecules. 2 We reported in the Proceedings of the National Academy of Sciences that HLA-E is an additional element greatly influencing the ability of CD8 + cytotoxic T lymphocytes (CTL) to respond to cancer cells. 3 HLA-E is a non-classical MHC class I molecule, which can bind a very limited variety of peptides, mainly derived from signal sequences of classical MHC class I peptides.…”