Host immunologic defenses are among the many systems profoundly altered as a result of thermal injury. Alterations in cell-mediated immunity, humoral immunity, the complement system, and phagocytic cells have been described extensively in the burn immunologic literature. Altered immune function following thermal injury results from a complex interaction of the components of the immune response as well as interaction of the metabolic alterations and the burn environment. The understanding and manipulation of the host defense mechanism is the next logical step in the control of infection following thermal injury. The etiology of the immune defects following thermal injury remains to be elucidated, however, it is clear from the burn immunologic literature that the defects can be produced by either an altered host environment or an injury-triggered host deficiency state. Whether alterations in immune functions is a deficiency disease or due to circulating toxins and factors or a combination of the two, it is now obvious that the final result is an over-stimulation of some immune system components suppressor T cell stimulation, complement activation and a depression of other components T helper cell, PMN function. During the past four years, we have investigated the altered internal environment in thermally injured patients and its effect on cell-mediated immunity, namely, suppressed lymphocyte response.