A major consequence of traumatic injury is immunosuppression. Findings from previous studies suggest that the depression of immune functions is severe in young males, ovariectomised and aged females. In contrast, the immune functions in proestrus females following trauma-haemorrhage are maintained. Studies have also shown that the survival rate in proestrus females following trauma-haemorrhage and the induction of subsequent sepsis is significantly higher than in age-matched males and ovariectomised females. Furthermore, administration of female sex hormone 17beta-oestradiol in males and ovariectomised females after trauma-haemorrhage prevents the suppression of immune response. Thus, these findings suggest that sex hormones play a significant role in shaping the host response following trauma. This article reviews studies delineating the mechanism by which sex hormones regulate immune cell functions in the experimental model of trauma-haemorrhage. The findings from the studies reviewed in this article suggest that sex steroids can be synthesised by the immune cell. The findings further indicate that T cell and macrophages express receptors for androgen and oestrogen. Since these cells are also the cells that produce cytokines, local synthesis of active steroids in these cells may become the significant factor in modulating their cytokine production.