Fig. 3

Mechanisms by which ISV initiates and stimulates an effective anti-tumor immune response. (a) Reversal of the immunosuppressive TME through the induction of proinflammatory cytokines, polarization of M2 pro-tumor macrophages into M1 anti-tumor macrophages, activation of DCs, and inhibition of immunosuppressive Tregs and MDSCs. (b–f) ICD-related mechanisms: (b) ICD leads to the release of tumor antigens (TAs); (c) recruitment, maturation, and activation of antigen-presenting cells (APCs) at the tumor site, enhancing TA uptake and antigen processing by APCs; (d) increased trafficking of APCs to lymph nodes, presentation or cross-presentation of TAs to T cells, activation of antigen-specific T cells, and differentiation into cytotoxic T lymphocytes (CTLs), T-helper (Th) cells, effector memory T cells (TEMs), central memory T cells (TCMs), and antibody-secreting B cells in the tumor-draining lymph node; (e) expansion and recruitment of immune cells, including CTLs, Th cells, NK cells, and granulocytes; (f) tumor targeting at distant sites by circulating effector T cells and antibodies, induction and activation of memory T cells (TEMs and TCMs), and establishment of long-term anti-tumor immune memory to prevent tumor relapse. Copyright 2018, Wiley Interdiscip Rev Nanomed Nanobiotechnol