Erratum: Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors

Nature Reviews. Cancer 6, 613–625 (2006)

There is an error in Figure 1 of this article on page 616. The mature immunogenic dendritic cell at the top of the figure should not be expressing IDO. The correct version of the figure is shown below.

Figure 1: Interactions between the tumour and cells of the immune system that foster an immunosuppressive microenvironment.

Through the production of cytokines (such as interleukin 10 (IL10), transforming growth factor β (TGFβ), IL13 and vascular endothelial growth factor (VEGF)) and chemokines (such as CCL22, CCL2 and CXCL12), tumours can promote the migration and expansion of cells that negatively regulate the immune system. T-regulatory (T_reg) cells, which block T-effector cells through both direct interaction and the production of immunosuppressive cytokines such as TGFβ and IL10, can be recruited as well as myeloid suppressor cells (MSCs), immature dendritic cells, natural killer T cells (NKTs) and tumour-associated macrophages (TAMs). These cells act to suppress the proliferation of effector-T cells (such as CD4⁺ helper T cells and CD8⁺ cytotoxic T cells), the production of cytokines (such as interferon γ (IFNγ) and IL2), and cytolytic activity. Both tumour cells and host cells can express enzymes that are involved in immune suppression (such as arginase (ARG), indoleamine 2,3-dioxygenase (IDO), cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS)). In addition, mature, toleragenic dendritic cells can also accumulate in tumour-draining lymph nodes. Induction of IDO activity in toleragenic DCs, through interaction with T_reg cells expressing cytotoxic-T-lymphocyte-associated antigen-4 (CTLA4), can promote further T_reg expansion and differentiation. CSF1, colony-stimulating factor-1; GMCSF, granulocyte-macrophage-CSF; PGE2, prostaglandin E2; ROS, reactive oxygen species; TDC, tumour-derived cytokine.