Exposure to cigarette smoke is known to suppress immune responses and to increase the incidence and severity of respiratory infections. In this study, we determined the effect of hydroquinone (HQ), which is found at high concentrations in cigarette smoke, on interferon-gamma ($IFN-{gamma}$) production by lymphocytes. HQ significantly inhibited $IFN-{gamma}$ secretion by keyhole limpet hemocyanin-primed lymphocytes in a dose-dependent manner. In addition, HQ inhibited $IFN-{gamma}$ secretion in effector $CD4^+$ T cells and Th1-differentiated $CD4^+$ T cells. The mRNA expression of $IFN-{gamma}$ and the $IFN-{gamma}$ gene promoter activity were inhibited by HQ. These results suggest that the inhibitory effect of HQ on $IFN-{gamma}$ secretion may occur at the transcriptional level. Furthermore, the effects of HQ on transcription factors were investigated. HQ inhibited the transcriptional activity of activator protein-1 and nuclear $factor-{kappa}B$, which are known to be involved in $IFN-{gamma}$ transcriptional activation. These findings provide evidence that HQ might suppress immune responses by reducing the production of $IFN-{gamma}$ and may explain the susceptibility to microbial infections caused by cigarette smoking.