Context: Preeclampsia represents a major cause of preterm birth, since definitive treatment demands fetal delivery. Although its pathophysiology is complicated, placental hypoxia and endothelial dysfunction constitute established pathogenetic steps of the disease. Inflammation is considered to be a crucial mediator of preeclampsia process, as an imbalance between TH1, TH2 and TH17 immune responses is observed. Objective: To evaluate the contribution of interleukins in preeclampsia, summarizing the pathways through which each interleukin exerts its function in the disease. Methods: The literature search was conducted using the MEDLINE (1966-2018) database, along with the reference list of the retrieved papers. The search strategy included the terms: “interleukin, tumor necrosis factor, TNF, TNF-α, inflammation, pre-eclampsia, preeclampsia, gestational hypertension”. Patients: 138 studies, assessing the role of interleukins in preeclampsia, were finally included in the present review. Intervention: Abstracts were screened and papers that were presumed to be eligible were retrieved as full-texts. Main Outcome Measures: Emphasis is given on the pathophysiological pathways, as well as the on the impact of gene polymorphisms on preeclampsia risk. Interleukin maternal serum levels are also examined, in order to explore their potential efficacy as predictive tools in the disease. Results: Preeclampsia is characterized by an imbalance between pro-inflammatory cytokines- such as IL-1, IL-6, IL-8, IL-17, and TNF-α-and anti-inflammatory regulatory interleukins, especially IL-10, IL-33, and IL-35. As a result, TH1 and TH17 responses are promoted and not counterbalanced by the deficient TH2 and Treg mechanisms. It is proposed that placental hypoxia leads to overexpression of pro-inflammatory cytokines, especially TNF-α, IL-6 and IL-17, which subsequently favor the production of reactive oxygen species, as well as the release of autoantibodies against angiotensin II type 1 receptor (AT1-AA), sFlt-1, soluble endoglin, and endothelin-1. The current evidence on the role of interleukin gene polymorphisms is controversial. Conclusions: The pathogenetic mechanisms in preeclampsia are based on impaired trophoblast invasion and the release of inflammatory and anti-angiogenic factors into the maternal circulation. Interleukins are not only responsible for the imbalance of immune responses, but they also promote placental ischemia and endothelial dysfunction.