In daily life, people are usually exposed to radiofrequency radiations (RFR). The effects of RFR on human physiology have been a major source of controversy since the WHO declared that these radiations are a type of environmental energy that interacts with the physiological functioning of the human body. The immune system provides internal protection and promotes long-term health and survival. However, the relevant research on the innate immune system and radiofrequency radiation is scant. In this connection, we hypothesized that innate immune responses would be influenced by exposure to non-ionizing electromagnetic radiation from mobile phones in a cell-specific and time-dependent manner. To test this hypothesis, human leukemia monocytic cell lines were exposed to 2318 MHz (MHz) RFR emitted by mobile phones at a power density of 0.224 W/m2 in a controlled manner for various time durations (15, 30, 45, 60, 90, and 120 min). Systematic studies on cell viability, nitric oxide (NO), superoxide (SO), pro-inflammatory cytokine production, and phagocytic assays were performed after the irradiation. The duration of exposure seems to have a substantial influence on the RFR-induced effects. It was noticed that after 30 min of exposure, the RFR dramatically enhanced the pro-inflammatory cytokine IL-1α level as well as reactive species such as NO and SO generation as compared to the control. In contrast, the RFR dramatically reduced the phagocytic activity of monocytes during 60 min of treatment when compared to the control. Interestingly, the irradiated cells restored their normal functioning until the final 120-min of exposure. Furthermore, mobile phone exposure had no influence on cell viability or TNF-α level. The results showed that RFR exhibits a time-dependent immune-modulatory role in the human leukemia monocytic cell line. Nevertheless, more research is needed to further determine the long-term effects and precise mechanism of action of RFR.Keywords: Free radical; Innate immune system; Monocytes; Nitrite; Non-ionizing electromagnetic radiation; Phagocytosis; Pro-inflammatory cytokine; Radiofrequency radiation; Superoxide.