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Interleukin-2 Receptor Expression and Function Following Thermal Injury

Diarmuid S. O'Riordain, MD; Manuel V. Mendez, MD; Rene G. Holzheimer, MD; Kathryn Collins; John A. Mannick, MD; Mary L. Rodrick, PhD
Arch Surg. 1995;130(2):165-170. doi:10.1001/archsurg.1995.01430020055009.
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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)


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