Evidence map›Paper›PMID 27026348›Full record

ReviewNature reviews. Nephrology2016

Role of TLRs and DAMPs in allograft inflammation and transplant outcomes.

Faouzi Braza, Sophie Brouard, Steve Chadban, Daniel R Goldstein

Abstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

93 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cellular and Molecular Aspects of Chronic Rejection.Results and problems in cell differentiation · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Unraveling CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Review
  13. Human type 1 conventional dendritic cells contribute to skin transplant rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Article
  14. Article
  15. Article
  16. Tissue-resident CCR2Cell reports · 2025
    Article
  17. Immunometabolism of Liver Xenotransplantation and Prospective Solutions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  18. Article
  19. Article
  20. Review

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Faouzi BrazaInstituto Gulbenkian de Ciência, Rua da Quinta Grande, 2780-156 Oeiras, Portugal.
Sophie BrouardINSERM, UMR 1064, CHU de Nantes, ITUN, 30 Bd Jean Monnet Nantes F-44093, France.
Steve ChadbanRenal Medicine and Transplantation, Royal Prince Alfred Hospital, Missenden Road Camperdown, NSW 2050, Sydney, Australia.
Daniel R GoldsteinDepartment of Internal Medicine, 333 Cedar St, Yale School of Medicine, New Haven, Connecticut 06525, USA.

Funding

Mechanisms to augment primary immunity in agingR01AG028082 · NIA · YALE UNIVERSITY · PI DENG, JANE C · 2007 to 2023
$6.9M
NIA NIH HHS R01 AG028082NIA NIH HHS R01AG028082
6 · The paper itself

Abstract

Graft inflammation impairs the induction of solid organ transplant tolerance and enhances acute and chronic rejection. Elucidating the mechanisms by which inflammation is induced after organ transplantation could lead to novel therapeutics to improve transplant outcomes. In this Review we describe endogenous substances--damage-associated molecular patterns (DAMPs)--that are released after allograft reperfusion and induce inflammation. We also describe innate immune signalling pathways that are activated after solid organ transplantation, with a focus on Toll-like receptors (TLRs) and their signal adaptor, MYD88. Experimental and clinical studies have yielded a large body of evidence that TLRs and MYD88 are instrumental in initiating allograft inflammation and promoting the development of acute and chronic rejection. Ongoing clinical studies are testing TLR inhibition strategies in solid organ transplantation, although avoiding compromising host defence to pathogens is a key challenge. Further elucidation of the mechanisms by which sterile inflammation is induced, maintained and amplified within the allograft has the potential to lead to novel anti-inflammatory treatments that could improve outcomes for solid organ transplant recipients.

Indexed as

AllograftsAnimalsHMGB1 ProteinHumansHyaluronic AcidImmunity, InnateInflammationMyeloid Differentiation Factor 88Organ TransplantationSignal TransductionToll-Like ReceptorsHMGB1 ProteinHyaluronic AcidMyeloid Differentiation Factor 88Toll-Like Receptors

Identifiers

PMID27026348
PMCPMC7952035

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.