Abstract
The tumour microenvironment (TME) presents a major block to anti-tumour immune responses and to effective cancer immunotherapy. The inflammatory mediators such as cytokines, chemokines, growth factors and prostaglandins generated in the TME alter the phenotype and function of dendritic cells (DCs) that are critical for a successful adaptive immune response against the growing tumour. In this mini review we discuss how tumour cells and the surrounding stroma modulate DC maturation and trafficking to impact T cell function. Fibroblastic stroma and the associated extracellular matrix around tumours can also provide physical restrictions to infiltrating DCs and other leukocytes. We discuss interactions between the inflammatory TME and infiltrating immune cell function, exploring how the inflammatory TME affects generation of T cell-driven anti-tumour immunity. We discuss the open question of the relative importance of antigen-presentation site; locally within the TME versus tumour-draining lymph nodes. Addressing these questions will potentially increase immune surveillance and enhance anti-tumour immunity.
Highlights
Anti-tumour immunity is the ability of the body’s immune system to recognise and eliminate tumour cells
It is established that tumours can exploit their surroundings to create an immunosuppressive microenvironment to control dendritic cells (DCs) function within both the tumour microenvironment (TME) and Tumour draining lymph node (TDLN) [178, 179]
The success of immunotherapy relies on enhanced T cell activity, activation of tumour-specific T cells cannot be achieved without prior antigen presentation by professional DCs
Summary
Stromal Immunology Laboratory, MRC Laboratory for Molecular Cell Biology, University College London, London, United Kingdom. Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal
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