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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Head Neck. 2018 Feb 20;40(6):1321–1334. doi: 10.1002/hed.25101

Figure 1. Summary of known innate immune signaling alterations following IR within the tumor microenvironment.

Figure 1

IR induces the release or surface translocation of several innate immune receptor ligands (HMGB1, ATP, CRT) in a process known as immunogenic cell death, that result in type I IFN production from antigen presenting cells (dendritic cells). Recent evidence also has demonstrated the importance of DNA sensing through cGAS, also resulting in STING-dependent type I IFN production. Type I IFN is critical for the maturation of dendritic cells, allowing cross-presentation of antigen and initiation of adaptive immunity. Activated T-cells in turn eliminate antigen positive target cells, but also help to reduce local immunosuppression through effector cytokine (IFNγ, TNFα)-dependent reduction in MDSCs. Whether IR can directly reduce the viability or function of immunosuppressive cells such as MDSCs, or whether this effect is secondary through T-cell effector cytokines, remains unclear.