Figure 6.

Graphical hypothesis. MOG immunization generates MOG-specific effector T cells that migrate to the CNS where they cause neuronal injury and induce neurons to express IDO1 and produce neurotoxic Trp catabolites such as QA (green highlights). STING agonists induce DCs in lymphoid tissues to express IDO1 and produce Trp catabolites that suppress generation of MOG-specific T cells (red highlights). Manipulating Trp catabolism to enhance production of immune suppressive catabolites and block production of neurotoxic catabolites may be an effective strategy to boost tolerogenic responses that promote stable EAE remission and alleviate neurologic comorbidities.