ReviewSeminars in immunopathology2008
Severe sepsis and Toll-like receptors.
Review in Seminars in immunopathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Special Issue "The Role of Toll-like Receptors (TLRs) in Infection and Inflammation: Third Edition".International journal of molecular sciences · 2026Article
- Special Issue "The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation 2.0".International journal of molecular sciences · 2024Article
- Cytokine storm and sepsis disease pathogenesis.Seminars in immunopathology · 2017Review
- Article
- The contribution of group A streptococcal virulence determinants to the pathogenesis of sepsis.Virulence · 2014Review
- LOX-1 deletion improves neutrophil responses, enhances bacterial clearance, and reduces lung injury in a murine polymicrobial sepsis model.Infection and immunity · 2011Article
- Alarmin HMGB1 is released in the small intestine of gnotobiotic piglets infected with enteric pathogens and its level in plasma reflects severity of sepsis.Journal of clinical immunology · 2011Article
- Effect of transforming growth factor-β1 on monocyte Toll-like receptor 4 expression in septic rats.World journal of emergency medicine · 2011Article
- Mortality in human sepsis is associated with downregulation of Toll-like receptor 2 and CD14 expression on blood monocytes.Diagnostic pathology · 2009Article
- Role of pulmonary intravascular macrophages in endotoxin-induced lung inflammation and mortality in a rat model.Respiratory research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe 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.
Indexed as
Identifiers
18071706What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.