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Review Open access

Immune function in burn patients: Pathophysiology, monitoring, and emerging therapeutic strategies.

Oct 2026 · Burns · Vol 52 9, pp. 108260 · 0 citations · 138 references
Medicine

Abstract

Severe burn injury causes extensive local tissue damage and systemic immune alterations that affect infection risk, wound healing, organ function, and survival. The immune response is characterized by rapid activation of innate immune cells, including neutrophils and monocytes, with elevated pro-inflammatory cytokines (IL‑6, TNF‑α, IL‑1β) and complement activity. Simultaneously, adaptive immunity is often impaired, with reduced T and B lymphocyte function, while diminished dendritic cell activity may further compromise antigen presentation and adaptive immune responses. This combined hyperinflammatory and immunosuppressive state, known as burn-induced immune dysfunction, contributes to delayed wound healing, increased susceptibility to secondary infections, sepsis, and multiple organ dysfunction. Monitoring immune function is essential but challenging. Routine markers, including white blood cell count (WBC) and C-reactive protein (CRP), provide limited insight, whereas procalcitonin (PCT), pancreatic stone protein (PSP), and cytokine panels (IL‑6, IL‑8, IL‑10) improve early detection of infection and immune classification. Flow cytometry allows characterization of immune cell populations and functional markers such as monocyte HLA‑DR and T cell PD‑1, while functional assays assess neutrophil, monocyte, and lymphocyte responsiveness. High-resolution molecular approaches, including transcriptomics, proteomics, and single-cell profiling, reveal persistent alterations not captured by conventional assays. Therapeutic strategies to restore immune balance include targeted cytokine modulation, immune checkpoint inhibition, hemoadsorption, metabolic and nutritional interventions, and novel approaches such as nanotechnology or microbiome modulation. Early surgical excision and topical treatments, including cerium-nitrate with silver sulfadiazine, may also attenuate systemic inflammation. However, robust clinical evaluation of these interventions is limited, and their timing, dosing, and patient selection remain under investigation. This review integrates mechanistic, translational, and clinical evidence to provide a framework for understanding burn-induced immune dysfunction. Future research should aim for standardized immune phenotyping, longitudinal multi-omics integration, AI-assisted monitoring, and evaluation of mechanism-based immunomodulatory strategies to improve patient outcomes.

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