Evidence map›Paper›PMID 18195076›Full record

ArticleThe Journal of experimental medicine2008

TLR-dependent cross talk between human Kupffer cells and NK cells.

Zhengkun Tu, Adel Bozorgzadeh, Robert H Pierce, Jonathan Kurtis, I Nicholas Crispe, Mark S Orloff

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
–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

109 citing papers in PubMed.

  1. Article
  2. Article
  3. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Tissue-Resident Immune Cells in Humans.Annual review of immunology · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Prediction and Prevention of Post-hepatectomy Liver Failure: Where Do We Stand?Journal of clinical and translational hepatology · 2021
    Article

49 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

6 authors.

Zhengkun TuDepartment of Surgery, Division of Solid Organ Transplantation and Hepatobiliary Surgery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Adel Bozorgzadeh
Robert H Pierce
Jonathan Kurtis
I Nicholas Crispe
Mark S Orloff

Funding

Puberty, Immunity and Malnutrition in S. JaponicumR01AI048123 · NIAID · RHODE ISLAND HOSPITAL · PI KURTIS, JONATHAN D. · 2001 to 2005
$3.0M
Kupffer Cells in Liver ImmunopathologyR01AI064463 · NIAID · UNIVERSITY OF ROCHESTER · PI CRISPE, IAN NICHOLAS · 2006 to 2010
$2.0M
NIAID NIH HHS AI064463NIAID NIH HHS R01 AI048123NIAID NIH HHS R01 AI064463NIAID NIH HHS R01-AI48123
6 · The paper itself

Abstract

The liver protects the host from gut-derived pathogens yet is tolerant of antigenic challenge from food and commensal sources. Innate responses involving liver macrophages (Kupffer cells) and effector liver natural killer (NK) cells form the first line in this defense. We address the impact of Toll-like receptor (TLR) signaling on the cross talk between these two cells, and reveal how the liver displays a down-regulated inflammatory response to constitutive bacterial elements through the secretion of interleukin (IL) 10 yet retains a vigorous response to viral challenge. The data support the model that (a) human liver Kupffer cells respond to TLR ligands and indirectly activate NK cells; (b) the activation depends on cell-cell contact; (c) the Kupffer cells synthesize NK cell activating signals, among which IL-18 is critical, and NK cell inhibitory factors, including IL-10; (d) ligands that signal via myeloid differentiation factor 88 induce IL-10, giving a blunted response in the NK cells; and (e) ligands that signal via the Toll-IL-1 receptor domain-containing adaptor inducing interferon (IFN) beta-IFN regulatory factor 3 pathway induce less IL-10, and also directly potentiate the stimulatory effect of IL-18 on NK cells, resulting in enhanced activation. Subversion of cellular mechanisms of innate immune response against viruses may be important for hepatotropic viruses (e.g., hepatitis B and C) to develop persistence.

Indexed as

CD56 AntigenCells, CulturedCoculture TechniquesHumansImmune SystemInterleukin-10Interleukin-18Killer Cells, NaturalKupffer CellsLigandsLipopolysaccharide ReceptorsLiverMacrophagesModels, BiologicalRecombinant ProteinsToll-Like ReceptorsCD56 AntigenInterleukin-10Interleukin-18LigandsLipopolysaccharide ReceptorsRecombinant ProteinsToll-Like Receptors

Identifiers

PMID18195076
PMCPMC2234385

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.