Evidence map›Paper›PMID 20146711›Full record

ReviewAnnals of the New York Academy of Sciences2010

Signaling of c-kit in dendritic cells influences adaptive immunity.

Prabir Ray, Nandini Krishnamoorthy, Timothy B Oriss, Anuradha Ray

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Detection ofInternational journal of molecular sciences · 2024
    Review
  7. Bone Marrow-Derived C-KitApplied biochemistry and biotechnology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 2 institutions in 1 country.

Prabir RayDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA. rayp@pitt.edu
Nandini Krishnamoorthy
Timothy B Oriss
Anuradha Ray
Pulmonary and Allergy Associates · USUniversity of Pittsburgh · US

Funding

Surrogate Biomarkers for Disease Progression in IPFP50HL084932 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PILEWSKI, JOSEPH MARK · 2006 to 2010
$12.2M
MECHANISMS OF ANTIGEN INDUCED TOLERANCE IN THE LUNGR01AI048927 · NIAID · YALE UNIVERSITY · PI RAY, ANURADHA · 2001 to 2020
$8.0M
DC-T Cell Interactions in Pulmonary Immune ResponsesR01HL077430 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RAY, ANURADHA · 2004 to 2012
$3.0M
KGF and Protection from Hyperoxic Lung InjuryR01HL069810 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RAY, PRABIR · 2001 to 2009
$2.7M
DIFFERENTIAL CHEMOKINE GENE EXPRESSION IN THE LUNGR01HL060207 · NHLBI · YALE UNIVERSITY · PI RAY, PRABIR · 1998 to 2008
$2.3M
NHLBI NIH HHS HL 060207NHLBI NIH HHS HL 069810NHLBI NIH HHS HL 077430NHLBI NIH HHS HL 084932NHLBI NIH HHS P50 HL084932NHLBI NIH HHS R01 HL060207NHLBI NIH HHS R01 HL069810NHLBI NIH HHS R01 HL077430NIAID NIH HHS AI 048927NIAID NIH HHS R01 AI048927
6 · The paper itself

Abstract

The binding of the receptor tyrosine kinase, c-kit, to its ligand, stem cell factor (SCF), mediates numerous biological functions. Important roles for c-kit in hematopoiesis, melanogenesis, erythropoiesis, spermatogenesis, and carcinogenesis are well documented. Similarly, activation of granulocytes, mast cells, and of eosinophils in particular, by c-kit ligation has long been known to result in degranulation with concomitant release of pro-inflammatory mediators, including cytokines. However, recent work from a number of laboratories, including our own, highlights previously unappreciated functions for c-kit in immunologic processes. These novel findings strongly suggest that signaling through the c-kit-SCF axis could have a significant impact on the pathogenesis of diseases associated with an immunologic component. In our own studies, c-kit upregulation on dendritic cells via T helper (Th)2- and Th17-inducing stimuli led to c-kit activation and immune skewing toward these T helper subsets and away from Th1 responses. Others have shown that dendritic cell treatment with inhibitors of c-kit activation, such as imatinib mesylate (Gleevec), favored breaking of T-cell tolerance, skewing of responses toward production of Th1 cytokines, and activation of natural killer cells. These data all indicate that deeper understanding of, and ability to control, the c-kit-SCF axis could lead to improved treatment modalities aimed at redirecting unwanted and/or deleterious immune responses in a wide variety of conditions.

Indexed as

Adaptive ImmunityAnimalsCell MembraneDendritic CellsHematopoietic Stem CellsHumansModels, BiologicalProtein IsoformsProto-Oncogene Proteins c-kitReceptors, NotchSignal TransductionStem Cell FactorProtein IsoformsProto-Oncogene Proteins c-kitReceptors, NotchStem Cell Factor

Identifiers

PMID20146711
PMCPMC3641791
OpenAlexW1583801395

What Socratic 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 Socratic graph.