Evidence map›Paper›PMID 23794631›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Th17 cells induce Th1-polarizing monocyte-derived dendritic cells.

Matthew G Davidson, Michael N Alonso, Robert Yuan, Robert C Axtell, Justin A Kenkel, Megan M Suhoski, Joseph C González, Lawrence Steinman, Edgar G Engleman

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. IL17FMolecular medicine (Cambridge, Mass.) · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Th17 Cells in Protection from Tumor or Promotion of Tumor Progression.Journal of clinical & cellular immunology · 2016
    Article
  10. A Distinct Region in Erythropoietin that Induces Immuno/Inflammatory Modulation and Tissue Protection.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
  11. Ablative Tumor Radiation Can Change the Tumor Immune Cell Microenvironment to Induce Durable Complete Remissions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. 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

9 authors at 2 institutions in 1 country.

Matthew G DavidsonDepartment of Pathology, Blood Center, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Michael N Alonso
Robert Yuan
Robert C Axtell
Justin A Kenkel
Megan M Suhoski
Joseph C González
Lawrence Steinman
Edgar G Engleman
Stanford University · USStanford Blood Center · US

Funding

TLI/ATG CONDTIONING: KIDNEY/BLOOD STEM CELL TRANSPLANTSP01HL075462 · NHLBI · STANFORD UNIVERSITY · PI ENGLEMAN, EDGAR G. · 2004 to 2020
$27.9M
Lupus Glomenulonephritis and NK T cellsR01DK082537 · NIDDK · STANFORD UNIVERSITY · PI STROBER, SAMUEL · 2009 to 2013
$2.3M
Defining Adaptive Immune Mechanisms of Insulin ResistanceR01DK096038 · NIDDK · STANFORD UNIVERSITY · PI ENGLEMAN, EDGAR G. · 2012 to 2015
$1.5M
NHLBI NIH HHS HL075462NHLBI NIH HHS P01 HL075462NIDDK NIH HHS DK082537NIDDK NIH HHS DK096038NIDDK NIH HHS R01 DK082537NIDDK NIH HHS R01 DK096038
6 · The paper itself

Abstract

In chronically inflamed tissues, such as those affected by autoimmune disease, activated Th cells often colocalize with monocytes. We investigate in this study how murine Th cells influence the phenotype and function of monocytes. The data demonstrate that Th1, Th2, and Th17 subsets promote the differentiation of autologous monocytes into MHC class II(+), CD11b(+), CD11c(+) DC that we call DCTh. Although all Th subsets induce the formation of DCTh, activated Th17 cells uniquely promote the formation of IL-12/IL-23-producing DCTh (DCTh17) that can polarize both naive and Th17 cells to a Th1 phenotype. In the inflamed CNS of mice with Th17-mediated experimental autoimmune encephalomyelitis, Th cells colocalize with DC, as well as monocytes, and the Th cells obtained from these lesions drive the formation of DCTh that are phenotypically indistinguishable from DCTh17 and polarize naive T cells toward a Th1 phenotype. These results suggest that DCTh17 are critical in the interplay of Th17- and Th1-mediated responses and may explain the previous finding that IL-17-secreting Th cells become IFN-γ-secreting Th1 cells in experimental autoimmune encephalomyelitis and other autoimmune disorders.

Indexed as

AnimalsAutoimmunityCD11b AntigenCD11c AntigenCell DifferentiationCell MovementCell PolarityCells, CulturedCentral Nervous SystemDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalFemaleHistocompatibility Antigens Class IIInflammationInterferon-gammaInterleukin-12CD11b AntigenCD11c AntigenHistocompatibility Antigens Class IIInterferon-gammaInterleukin-12Interleukin-17Interleukin-23

Identifiers

PMID23794631
PMCPMC3954848
OpenAlexW2102096193

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.