T-cell reactivity and its predictive role in immunosuppression after burns

Area of Science:

• Immunology
• Trauma Research
• Cellular Biology

Background:

• Trauma, particularly major burns, can induce significant immune system alterations.
• Understanding T-helper cell responses (T(H)1 and T(H)2) is crucial for predicting patient outcomes.
• Previous research suggests a shift towards T(H)2 dominance increases postburn infection risk.

Purpose of the Study:

• To investigate constitutional and phenotype-dependent changes in T-helper-1 (T(H)1) and T-helper-2 (T(H)2) lymphokine synthesis after major burn injury.
• To identify the specific T-cell subsets responsible for altered cytokine production post-trauma.

Main Methods:

• A prospective, descriptive study involving ten major burn patients and fifteen healthy controls.
• Peripheral blood mononuclear cells were isolated and stimulated to assess cytokine production (Interferon-gamma [IFN-γ] and Interleukin-4 [IL-4]).
• Immunofluorescent staining identified T-cell phenotypes (CD4, CD8) and intracellular cytokine expression, correlated with ELISA measurements.

Main Results:

• Burn patients showed similar CD4+ and CD8+ T-cell percentages compared to controls.
• A significant up-regulation of IL-4 production was observed, predominantly from CD8+ T-cells.
• IFN-γ release was only slightly increased, with CD4+ T-cells showing minimal change; however, CD8+ cells showed increased IFN-γ.
• Nonsurvivors had higher numbers of CD8+ IL-4-producing cells and lower numbers of IFN-γ-releasing CD4+ T-cells compared to survivors.

Conclusions:

• Major burns induce a significant shift in cytokine response towards T(H)2, primarily mediated by CD8+ T-cells.
• This T(H)2-dominant profile, characterized by increased IL-4, is associated with immunosuppression and a higher risk of postburn infections.
• These findings may aid in differentiating inflammatory states and contraindicate anti-inflammatory therapy for sepsis in burn patients.