Taken together, an immune response resulting in the increased production of proinflammatory cytokines may induce symptoms of depression, predominantly via central neuroinflammation; a reduction in tryptophan availability, resulting in serotonin depletion along IDO activation; increased production of kynurenine neurotoxic metabolites; and HPA axis overdrive, including glucocorticoid-receptor downregulation. This evidence concerns the gene IDO1 and depressive symptom measurement.