Large numbers of reports have shown that thermal injury (TI) causes a wide spectrum of defects in immune response that lead to a high susceptibility to various opportunistic infections. However, it is still a matter of debate whether TI induces Th2 polarization or global impairment in Th1/Th2 response. In this study, TI in a mouse model was induced by exposing shaved dorsal skin to boiling water and cytokine production was analyzed. At day 2 of injury, whole spleen cells and T cells were collected and then stimulated with an anti-CD3 antibody. The levels of cytokine secretion were determined by cytokine ELISA. Production of $IFN{gamma}$ and IL 4 by whole spleen cells from injured mice were concurrently decreased when compared to those from sham-injured controls. Proportional changes in T, B, and T-subset cells were not accompanied. Using purified T cells devoid of accessory cells (AC), it was shown that those defects resulted primarily from lowered T cell potentials. By using mixed cultures of sham T and TI-AC and vice versa, it was revealed that AC also acted as inhibitor cells in $IFN{gamma}$ and IL 4 production in less extent. Blockade of glucocorticoid signals rendered the T cells partially resistant to TI-induced inhibition in $IFN{gamma}$ and but not IL 4 production. These results clearly demonstrate that TI induces overall suppression in Thl and Th2 response through T cell dysfunction together with the inhibition of AC activity, and that reduction in only $IFN{gamma}$ but not IL 4, production may be caused, in part, by corticosteroid hormone that is secreted prominently during trauma.