Background/Objective: Serious traumatic or thermal injury is associate
d with depression of cellular immunity, including the failure of T-lym
phocyte 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 thi
s issue. Design: A total of 20 male A/J mice (n=22 per group) were sub
jected to a 20% scald burn injury or sham burn, killed 4, 7, 10, 14, o
r 21 days later, and splenocytes harvested. In vitro parameters of bot
h IL-2R expression and function were measured. Results: On day 7, sple
nic lymphocyte proliferation and IL-2 production in response to mitoge
nic 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 stimulatio
n on days 7, 10, and 14 in thermally injured animals. Phenotypic IL-2R
p55 expression in concanavalin A-stimulated CD3(+) cells was unchange
d following burn injury. Binding of fluorescein-labeled IL-2 to cell m
embranes was increased in burned animals at days 10 and 14. The additi
on of IL-2 to cultures of spleen cells from burned mice consistently r
estored the mitogenic response to that of the controls. Conclusions: T
hermal 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 relate
d to abnormal IL-2 production.