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Effect of human recombinant interleukin (IL-2) on peripheral blood mononuclear cells of burned patients
Interleukin-2 (IL-2) has been suggested to play a key role in the immune response. To investigate the effect of human recombinant IL-2 on proliferative and cytotoxic responses in burn patients, peripheral blood mononuclear cells from 20 severely burned patients (body surface area (BSA) greater than 20 per cent) were studied in this way. Proliferative response measured by tritiated thymidine uptake was impaired from week 2 following injury. IL-2-activated cytotoxicity to NK-resistant target T24 was significantly impaired from week 2. To clarify if the defect in cytotoxic response is due to a decreased number of cell precursors or due to reduced responsiveness to IL-2, a limiting dilution assay was introduced. However, there was no reduction in precursor cell numbers. These data suggest that, in addition to impaired IL-2 production, there is an endogenous defect in IL-2 responsiveness. This may be of clinical importance since it is not possible to reverse this defect, at least in vitro.
Interleukin-2 (IL-2) has been suggested to play a key role in the immune response. To investigate the effect of human recombinant IL-2 on proliferative and cytotoxic responses in burn patients, peripheral blood mononuclear cells from 20 severely burned patients (body surface area (BSA) greater than 20 per cent) were studied in this way. Proliferative response measured by tritiated thymidine uptake was impaired from week 2 following injury. IL-2-activated cytotoxicity to NK-resistant target T24 was significantly impaired from week 2. To clarify if the defect in cytotoxic response is due to a decreased number of cell precursors or due to reduced responsiveness to IL-2, a limiting dilution assay was introduced. However, there was no reduction in precursor cell numbers. These data suggest that, in addition to impaired IL-2 production, there is an endogenous defect in IL-2 responsiveness. This may be of clinical importance since it is not possible to reverse this defect, at least in vitro.