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- Hongmei Gao, Susannah K Leaver, Anne Burke-Gaffney, and Simon J Finney.
- Unit of Critical Care Medicine, National Heart and Lung Institute, Imperial College, London, UK.
- Semin Immunopathol. 2008 Feb 1;30(1):29-40.
AbstractSevere sepsis dominates the mortality of non-cardiac intensive care units. The ingenious Toll-like receptor (TLR) system can recognise many infectious organisms through relatively few receptors to trigger pro-inflammatory and anti-inflammatory cytokine release. Further complexity arises from positive and negative signalling feedback loops. Severe sepsis may be a consequence of an inappropriately excessive response or inadequate endogenous negative feedback. Therapies targeting these pathways are currently being evaluated. Alternatively, in clinical scenarios such as compensatory anti-inflammatory response syndrome, chronic viral sepsis or inadequate vaccine function, TLR signalling may be inadequate. TLR agonists may augment the innate response and are being investigated.
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