February 1995

Interleukin-2 Receptor Expression and Function Following Thermal Injury

Author Affiliations

From the Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. Dr O'Riordain is now with the Department of Surgery, University Hospital of Cork, Wilton, Cork, Ireland.

Arch Surg. 1995;130(2):165-170. doi:10.1001/archsurg.1995.01430020055009

Background/Objective:  Serious traumatic or thermal injury is associated with depression of cellular immunity, including the failure of T-lymphocyte proliferation in response to stimulation that depends both on production of interleukin-2 (IL-2) and on expression of functional IL-2 receptors (IL-2R). While decreased IL-2 production following thermal injury is undisputed, the status of IL-2R expression and function in this setting is controversial; therefore, we sought to investigate this issue.

Design:  A total of 220 male A/J mice (n=22 per group) were subjected to a 20% scald burn injury or sham burn, killed 4, 7, 10, 14, or 21 days later, and splenocytes harvested. In vitro parameters of both IL-2R expression and function were measured.

Results:  On day 7, splenic lymphocyte proliferation and IL-2 production in response to mitogenic stimulation were both suppressed following burn injury to 50% and 60% of controls, respectively. Northern blot analysis revealed normal IL-2R p55 messenger RNA expression in response to mitogenic stimulation on days 7, 10, and 14 in thermally injured animals. Phenotypic IL-2R p55 expression in concanavalin A–stimulated CD3+ cells was unchanged following burn injury. Binding of fluoresceinlabeled IL-2 to cell membranes was increased in burned animals at days 10 and 14. The addition of IL-2 to cultures of spleen cells from burned mice consistently restored the mitogenic response to that of the controls.

Conclusions:  Thermal injury in this model does not result in either quantitative or functional suppression of IL-2R. Suppression of T-cell activation and proliferation, seen following thermal injury, appears primarily related to abnormal IL-2 production.(Arch Surg. 1995;130:165-170)