Dysregulation of inflammation in depression has knock-on effects on reward processing: transiently increasing inflammatory cytokines such as interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) decreases reward responsivity in the ventral striatum, as well as dopamine transmission in the caudate and putamen and increases depressive symptoms including anhedonia [132, 133]; and ventral striatal response to reward anticipation has been reported to mediate the effect of inflammation on mood [134]. Here, IL6 is linked to depressive disorder.