AFTER SEVERE injuries, dysbalanced cytokine synthesis contributes to dysregulated immune functions and to enhanced susceptibility toward microbial infections. During the past decade, the pattern of helper T cells type 1 (T
H1) and type 2 (T
H2) has been recognized as a fundamental principle of T-cell responses.
1 Helper T cells type 1 are potent producers of interleukin 2 (IL-2) and interferon γ (IFN-γ); in contrast, T
H2 cells produce IL-4, IL-5, or IL-13.
2 Intracellular staining of cytokine generation in activated T cells has emerged as a powerful tool to discriminate T
H1 and T
H2 cells using flow cytometry.
2 Recently, several studies
3-6 have described distinct alterations in the T
H1-T
H2 ratio of peripheral lymphocytes obtained from severely burned and surgical patients. Whereas after severe burn trauma a clear increase in T
H2 cells but no decrease in T
H1 cells has been reported,
5,6 different observations were made in surgical patients. No increase in T
H2 cells but a significant decrease in T
H1 cells has been observed after conventional hernia repair.
3 An increased or unaltered release of IL-4 has been reported
7,8 from isolated lymphocytes after conventional cholecystectomy, accompanied by a decrease in the release of IL-2 or IFN-γ, respectively. In addition, it was shown
9 that cytokine release from T
H1 and T
H2 cells was concomitantly diminished in severely injured patients with trauma. Furthermore, in vivo exposure of healthy individuals to endotoxin led to reduced production of T
H1 cytokines but not to an increase in T
H2 cytokines from stimulated whole blood.
10 Because of similar conflicting results obtained in animal trauma models,
11-13 the effect of severe injuries on the T
H1/T
H2 pattern remains unclear.