Evidence map›Paper›PMID 10619859›Full record

ArticleThe Journal of clinical investigation2000

Targeting of the chemokine receptor CCR1 suppresses development of acute and chronic cardiac allograft rejection.

W Gao, P S Topham, J A King, S T Smiley, V Csizmadia, B Lu, C J Gerard, W W Hancock

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
11.3field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 251 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The role of macrophages in thermal injury.International journal of burns and trauma · 2022
    Review
  6. Review
  7. Article
  8. The chemokines CCR1 and CCRL2 have a role in colorectal cancer liver metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Chemokines and transplant vasculopathy.Circulation research · 2008
    Review
  19. Article
  20. Deletion of the chemokine receptor CCR1 prolongs corneal allograft survival.Investigative ophthalmology & visual science · 2007
    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

8 authors at 4 institutions in 1 country.

W GaoLeukoSite Inc., Cambridge, Massachusetts 02142, USA.
P S Topham
J A King
S T Smiley
V Csizmadia
B Lu
C J Gerard
W W Hancock
KalVista Pharmaceuticals (United States) · USBoston Children's Hospital · USBoston University · USHarvard University · US

Funding

NUCLEAR FACTOR KAPPA BETA DEPENDENT GENES AND TRANSPLANT ARTERIOSCLEROSISP01AI040152 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI TILNEY, NICHOLAS L · 1996 to 2000
$798k
NIAID NIH HHS P01-AI40152
6 · The paper itself

Abstract

Although mononuclear cell infiltration is a hallmark of cellular rejection of a vascularized allograft, efforts to inhibit rejection by blocking leukocyte-endothelial cell adhesion have proved largely unsuccessful, perhaps in part because of persistent generation of chemokines within rejecting grafts. We now provide, to our knowledge, the first evidence that in vivo blockade of specific chemokine receptors is of therapeutic significance in organ transplantation. Inbred mice with a targeted deletion of the chemokine receptor CCR1 showed significant prolongation of allograft survival in 4 models. First, cardiac allografts across a class II mismatch were rejected by CCR1(+/+) recipients but were accepted permanently by CCR1(-/-) recipients. Second, CCR1(-/-) mice rejected completely class I- and class II-mismatched BALB/c cardiac allografts more slowly than control mice. Third, levels of cyclosporin A that had marginal effects in CCR1(+/+) mice resulted in permanent allograft acceptance in CCR1(-/-) recipients. These latter allografts showed no sign of chronic rejection 50-200 days after transplantation, and transfer of CD4(+) splenic T cells from these mice to naive allograft recipients significantly prolonged allograft survival, whereas cells from CCR1(+/+) mice conferred no such benefit. Finally, both CCR1(+/+) and CCR1(-/-) allograft recipients, when treated with a mAb to CD4, showed permanent engraftment, but these allografts showed florid chronic rejection in the former strain and were normal in CCR1(-/-) mice. We conclude that therapies to block CCR1/ligand interactions may prove useful in preventing acute and chronic rejection clinically.

Indexed as

Acute DiseaseAnimalsChronic DiseaseCyclosporineGraft RejectionGraft SurvivalHeart TransplantationLymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, CCR1Receptors, ChemokineRNA, MessengerTransplantation, HomologousCcr1 protein, mouseCyclosporineReceptors, CCR1Receptors, ChemokineRNA, Messenger

Identifiers

PMID10619859
PMCPMC382589
OpenAlexW1985277568

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.