Background　Comorbidity of neuropathic pain and depression seriously affects life quality. Recent studies have found that cytokines play important roles in the pathogenesis of neuropathic pain-depression comorbidity.　Objective　To review the effects of inflammatory cytokines on neuropathic pain-depression comorbidity, which will provide clues for effective prevention and treatment of the comorbidity.　Content　Neuropathic pain is associated with injuries and dysfunctions of somatosensory nervous system, and consists of a series of pain symptoms, including allodynia, pain hypersensitivity, and spontaneous pain, etc. Depression is a state of low mood and aversion to activity. Following activation of microglia, many inflammatory cytokines, such as, TNF-α, IL-1β, and IL-6, elevate and subsequently exacerbate both neuropathic pain and depression by interacting with 5-HT receptors, glutamate receptors, γ-aminobutyric acid receptors, and promoting activation of hypothalamus-pituitary-adrenaline axis.　Trend　Inflammatory cytokines may be potential targets for the treatment of neuropathic pain-depression comorbidity.