Lack of effect of exogenous recombinant interleukin-2 on trauma-induced abnormalities in lymphocyte proliferation.
Injury impairs cell-mediated immune function by depressing mitogen-induced lymphocyte proliferation and decreasing interleukin-2 (IL-2) production. In this study, we examined the ability of exogenous, recombinant IL-2 to restore lymphocyte proliferation after trauma. Recombinant IL-2 was added to cultures of phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells obtained from seven healthy volunteers and from 21 victims of accidental trauma. In comparison to the healthy group, lymphocyte proliferation was reduced approximately 20% in patients with minor and moderate injuries, and 50% in patients with severe injuries. The addition of recombinant IL-2 to PHA-stimulated lymphocytes from injured patients did not substantially improve cellular proliferation. These results suggest that the depressed response of lymphocytes to mitogen stimulation after trauma is not due to decreased IL-2 generation.
D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins; D011994:Recombinant Proteins / Q000494:pharmacology*; D012720:Severity of Illness Index; D014947:Wounds and Injuries / Q000276:immunology*
D007376:Interleukin-2; D010835:Phytohemagglutinins; D011994:Recombinant Proteins