In chronic hepatitis B virus (HBV)-infected patients, T helper 17 (Th17) cells are significantly elevated. Th17 cells initiate immune-mediated pathogenesis and have a critical role in the process of HBV-related liver cirrhosis (HBV-LC). The mechanisms underlying this process are attributed to Th17-secreted cytokines, which include interleukin (IL)-17, IL-21 and IL-22; however, a systemic analysis regarding these mechanisms has yet to be conducted. Therefore, the present study aimed to investigate the role of Th17 cells in the pathogenesis of HBV-LC. All randomized clinical trials, case series, case reports and meta-analyses that contained the aforementioned keywords were included in the review process. In addition, unpublished information from the Food and Drug Administration was included. The findings indicated that Th17-secreted cytokines, including IL-17, IL-21 and IL-22, function by activating or silencing hepatic stellate cells, modulating proinflammatory and pro-or antifibrogenic effectors, regulating extracellular matrix formation, upregulating chemokine expression, and inducing hepatocellular damage or hepatoprotection during the HBV-LC process. In addition, Th17 cells and Th17-secreted cytokines may be considered a potential tool in the diagnosis or treatment of HBV-LC. The present review summarized the role of Th17 cells in the pathogenesis of HBV-LC in order to deepen the clinical understanding of the role of Th17 cells and also to support the development of effective therapies for patients with HBV-LC.