Nerve injury is a significant cause of postherpetic neuralgia (PHN). It is marked by upregulated expression of cytokines secreted by immune cells such as tumor necrosis factor alpha, interleukin 1 beta (IL-1β), IL-6, IL-18, and IL-10. In neuropathic pain (NP) due to nerve injury, cytokines are important for the induction of neuroinflammation, activation of glial cells, and expression of cation channels. The release of chemokines due to nerve injury promotes immune cell infiltration, recruiting inflammatory cytokines and further amplifying the inflammatory response. The resulting disequilibrium in neuroimmune response and neuroinflammation leads to a reduction of nerve fibers, altered nerve excitability, and neuralgia. PHN is a typical NP and cytokines may induce PHN by promoting central and peripheral sensitization. Currently, treating PHN is challenging and research on the role of cytokine signaling pathways in PHN is lacking. This review summarizes the potential mechanisms of cytokine-mediated PHN and discusses the cytokine signaling pathways associated with the central and peripheral sensitization of PHN. By elucidating the mechanisms of cytokines, the cells and molecules that regulate cytokines, and their signaling systems in PHN, this review reveals important research developments regarding cytokines and their signaling pathways mediating PHN, highlighting new targets of action for the development of analgesic drugs.