Figure 2.

Chemokine network in the tumoral microenvironment immune response. Immune cells with antitumor effects such as CD8⁺ T cells, T_H1 cells, polyfunctional T_H17 cells and NK cells are attracted to the chemokine–chemokine receptor signalling pathways. CXCR3 and its ligands CXCL9 and CXCL10 have a main role in driving the migration of T_H1 cells, CD8⁺ T cells and NK cells into the TME, while CCL20 signalling through CCR6 promotes the recruitment of T_H17 cells. Furthermore, antigen presenting cells including macrophages and dendritic cells are also recruited into the TME, where they can activate and expand the local effector immune cells, promoting tumor regression. In turn, immune cell populations such as MDSCs, T_reg cells, T_H22 cells, IL-22⁺ innate lymphoid cells (ILCs) and plasmocytic dendritic cells can promote tumor growth. These cells are recruited to the tumor bed in response to different chemokines that are expressed in the TME (the relevant receptors and ligands are shown). Immune cells with pro-tumorigenic actions may hinder antitumor immune responses and may also mediate and sustain cancer stemness and angiogenesis, resulting in cancer progression.