Evidence map›Paper›PMID 11035738›Full record

ArticleInfection and immunity2000

Mononuclear cell recruitment, granuloma assembly, and response to treatment in experimental visceral leishmaniasis: intracellular adhesion molecule 1-dependent and -independent regulation.

H W Murray

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 14% of its field
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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role of Cytokines in Experimental and Human Visceral Leishmaniasis.Frontiers in cellular and infection microbiology · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Liposomal resiquimod for the treatment of Leishmania donovani infection.The Journal of antimicrobial chemotherapy · 2014
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

H W MurrayDepartment of Medicine, Weill Medical College of Cornell University, New York, New York 10021, USA. hwmurray@med.cornell.edu
Cornell University · US

Funding

MONONUCLEAR PHAGOCYTE KILLING OF LEISHMANIA PARASITESR01AI016963 · NIAID · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MURRAY, HENRY W. · 1985 to 2005
$2.9M
Host Immunoregulation of Response to Antileishmanial ChemotherapyR56AI016963 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI MURRAY, HENRY W. · 2007 to 2007
$420k
NIAID NIH HHS AI 16963NIAID NIH HHS R01 AI016963NIAID NIH HHS R56 AI016963
6 · The paper itself

Abstract

In experimental visceral leishmaniasis, acquired resistance to intracellular Leishmania donovani is Th1 cell cytokine dependent and largely mediated by gamma interferon (IFN-gamma); the same response also permits conventional antimony (Sb) chemotherapy to express its leishmanicidal effect. Since the influxing blood monocyte (which utilizes endothelial cell ICAM-1 for adhesion and tissue entry) is a primary effector target cell for this cytokine mechanism, we tested the monocyte's role in host responsiveness to chemotherapy in mice with ICAM-1 gene disruptions. Mutant animals failed to develop any early granulomatous tissue response in the liver, initially supported high-level visceral parasite replication, and showed no killing after Sb treatment; the leishmanicidal response to a directly acting, alternative chemotherapeutic probe, amphotericin B, was intact. However, mutant mice proceeded to express a compensatory, ICAM-1-independent response leading to mononuclear cell influx and granuloma assembly, control over visceral infection, and the capacity to respond to Sb. Together, these results point to the recruitment of emigrant monocytes and mononuclear cell granuloma formation, mediated by ICAM-1-dependent and -independent pathways, as critical determinants of host responsiveness to conventional antileishmanial chemotherapy.

Indexed as

AnimalsAntimonyCell MovementGranulomaIntercellular Adhesion Molecule-1Interferon-gammaLeishmaniasis, VisceralLeukocytes, MononuclearMiceMice, Inbred C57BLMonocytesT-LymphocytesAntimonyIntercellular Adhesion Molecule-1Interferon-gamma

Identifiers

PMID11035738
PMCPMC97712
OpenAlexW2101368042

What OpenQuestion holds

Textmetadata
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.