Immunomodulation in Sepsis-Induced Immunosuppression
Summary
Sepsis arises from a dysregulated host response to infection, transitioning from an early hyperinflammatory phase to profound immunosuppression. This immunosuppression is characterised by loss of lymphocyte function, increased apoptosis of T cells, expansion of regulatory cell populations and expression of inhibitory checkpoint molecules. Restoration of immune competence through targeted immunomodulation offers a promising route to reduce mortality, prevent secondary infections and improve long-term outcomes. Approaches under investigation include selective enhancement of autophagic processes in immune cells, blockade of co-inhibitory pathways to reverse lymphocyte exhaustion, and delivery of cytokines or growth factors to rebalance immune activation. Precision in immune stratification is essential, as interventions must be timed and tailored to individual trajectories of immune dysfunction. Advances in understanding cellular programmes such as ribophagy, innate lymphoid cell function and checkpoint regulation are driving the development of novel therapies that aim to re-establish immune homeostasis without rekindling damaging inflammation.
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Immunomodulation in Sepsis-Induced Immunosuppression publication trend
The graph below shows the total number of articles in immunomodulation in sepsis-induced immunosuppression across all publications each year (not limited to Nature Index journals).
Technical terms
Immunosuppression: A state of reduced immune competence, often following an initial hyperinflammatory response in sepsis.
Ribophagy: Selective autophagy of ribosomes that maintains cellular homeostasis and protects immune cells from stress-induced apoptosis.
T-lymphocyte apoptosis: Programmed cell death of T cells, contributing to impaired adaptive immunity in sepsis.
Programmed death-1 (PD-1): An inhibitory receptor on T cells that mediates immune checkpoint regulation and contributes to T cell exhaustion.
Programmed death ligand-1 (PD-L1): Ligand for PD-1 expressed on various cells; its engagement suppresses T cell activation.
Innate lymphoid cell type 2 (ILC2): A subset of innate immune cells producing type 2 cytokines, involved in tissue repair and regulation of inflammation.
References
- Nuclear fragile X mental retardation-interacting protein 1-mediated ribophagy protects T lymphocytes against apoptosis in sepsis. Burns & Trauma (2023).
- Roles of programmed death‐1 and muscle innate lymphoid cell‐derived interleukin 13 in sepsis‐induced intensive care unit‐acquired weakness. Journal of Cachexia Sarcopenia and Muscle (2024).
- Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options. Military Medical Research (2022).
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