Evidence map›Paper›PMID 18716926›Full record

ArticleExperimental lung research2008

CXCR3 ligands contribute to Th1-induced inflammation but not to homing of Th1 cells into the lung.

Anne M Manicone, Kristi M Burkhart, Bao Lu, Joan G Clark

Open access · greenAbstract read
In one paragraph

Article in Experimental lung research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. M1Journal for immunotherapy of cancer · 2020
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Pulmonary T cell activation in response to chronic particulate air pollution.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Innate immunity in the respiratory epithelium.American journal of respiratory cell and molecular biology · 2011
    Review
  15. Review
  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

4 authors at 3 institutions in 1 country.

Anne M ManiconeDivision of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, and Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. manicone@u.washington.edu
Kristi M Burkhart
Bao Lu
Joan G Clark
University of Washington · USBoston Children's Hospital · USFred Hutch Cancer Center · US

Funding

RESPIRATORY RESEARCH TRAINING PROGRAMT32HL007287 · NHLBI · UNIVERSITY OF WASHINGTON · PI Kristina Anne Crothers, David J. Horne · 1985 to 2026
$16.7M
CD154-CD13 Pathway in Inflammation-driven AngiogenesisR01HL069442 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI SHAPIRO, LINDA H · 2001 to 2004
$1.3M
Lymphocyte Trafficking in Th1 Cell Mediated Lung InjuryR01HL069422 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI CLARK, JOAN G. · 2001 to 2004
$1.2M
Role of CXCR3 in Th1-Mediated Lung InjuryF32HL078110 · NHLBI · UNIVERSITY OF WASHINGTON · PI MANICONE, ANNE M · 2004 to 2004
$42k
NHLBI NIH HHS F32 HL078110NHLBI NIH HHS F32-HL078110NHLBI NIH HHS R01 HL069422NHLBI NIH HHS R01 HL069442NHLBI NIH HHS R01-HL069442NHLBI NIH HHS T32 HL007287NHLBI NIH HHS T32-HL07287
6 · The paper itself

Abstract

Th1 cells are implicated in numerous pulmonary inflammatory disorders, and adoptive transfer of alloreactive Th1 cells mediates lung injury and inflammation in mice. In response to Th1-mediated immune injury, CXCR3 ligands IP10 and MIG are markedly induced. Because Th1 cells express high levels of CXCR3, their recruitment and activity may be influenced by CXCR3 ligands. To examine the role of CXCR3 ligands, the authors inhibited CXCR3-ligand interaction by 2 approaches: (1) antibody ablation of CXCR3 ligands IP10 (CXCL10/interferon-gamma -inducible 10-kDa protein) and MIG (CXCL9/monokine-induced by interferon-gamma), and (2) use of cxcr3(-/-) mice. Antibody neutralization of IP10 and MIG reduced Th1-cell mediated lung inflammation but did not alter Th1-cell influx in the lung. In contrast, a lack of CXCR3 on host cells had no effect on Th1 cells influx or acute inflammation. In vitro, ablation of endogenous IP10 and MIG inhibited antigen-mediated Th1-cell proliferation. These results suggest that the influx of alloreactive Th1 cells into the lung does not require CXCR3 ligands, but that these chemokines do affect Th1-cell proliferation and activity within the affected tissue. Other CXCR3(+) leukocytes do not contribute to acute alloimmune injury.

Indexed as

Chemotaxis, LeukocyteAdoptive TransferAnimalsAntibodiesCell ProliferationCells, CulturedChemokine CXCL10Chemokine CXCL9Disease Models, AnimalLigandsLungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutPneumoniaAntibodiesChemokine CXCL10Chemokine CXCL9Cxcl10 protein, mouseCxcl9 protein, mouseCxcr3 protein, mouseLigandsReceptors, CXCR3Recombinant Proteins

Identifiers

PMID18716926
PMCPMC2820292
OpenAlexW2058641049

What OpenQuestion holds

Textmetadata
LicenceTDM
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.