In this way, depression related pro-inflammatory Th1 responses (e.g., IDO activation and 5-HT depletion), of which IFN-γ is the principal effector, could become accentuated at the expense of anti-inflammatory Th2 ones (e.g., those mediated by IL-4 and IL-10; Najjar et al., 2013). The gene discussed is IFNG; the disease is depressive symptom measurement.