Since peripheral l-KYN and 3-hydroxy-l-kynurenine (3-HK) can enter the CNS via the blood brain barrier (Vecsei et al., 2013), central and/or peripheral activation of IDO and the formation of neurotoxic catabolites in response to increased inflammatory activity may account for the adverse innate and adaptive immune effects and the perpetuation of other central immune-induced changes, such as serotonin deficiency associated with depression (Dantzer et al., 2011). This evidence concerns the gene IDO1 and depressive symptom measurement.