Evidence map›Paper›PMID 22231518›Full record

ArticleNature immunology2012

Signaling via the kinase p38α programs dendritic cells to drive TH17 differentiation and autoimmune inflammation.

Gonghua Huang, Yanyan Wang, Peter Vogel, Thirumala-Devi Kanneganti, Kinya Otsu, Hongbo Chi

Abstract read
In one paragraph

Article in Nature immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Review
  3. Effects ofMetabolites · 2025
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  16. Critical role of metabotropic glutamate receptor 4 in bone marrow-derived dendritic cells in the Th17 cell differentiation and the melanogenesis of B16 cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  17. Article
  18. Review
  19. Protein kinase p38α signaling in dendritic cells regulates colon inflammation and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 3 countries.

Gonghua HuangDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Yanyan Wang
Peter Vogel
Thirumala-Devi Kanneganti
Kinya Otsu
Hongbo Chi
St. Jude Children's Research Hospital · USOsaka University · JP

Funding

The MKP-1/p38 axis: coordinating innate and adaptive immunityR01NS064599 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHI, HONGBO · 2008 to 2018
$3.7M
Sphingosine 1-Phosphate Signaling in Autoimmune RegulationK01AR053573 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHI, HONGBO · 2007 to 2011
$770k
NIAMS NIH HHS K01 AR053573NINDS NIH HHS R01 NS064599
6 · The paper itself

Abstract

Dendritic cells (DCs) bridge innate and adaptive immunity, but how DC-derived signals regulate T cell lineage choices remains unclear. We report here that the mitogen-activated protein kinase p38α programmed DCs to drive the differentiation of the T(H)17 subset of helper T cells. Deletion of p38α in DCs protected mice from T(H)17 cell-mediated autoimmune neuroinflammation, but deletion of p38α in macrophages or T cells did not. We also found that p38α orchestrated the expression of cytokines and costimulatory molecules in DCs and further 'imprinted' signaling via the receptor for interleukin 23 (IL-23R) in responding T cells to promote T(H)17 differentiation. Moreover, p38α was required for tissue-infiltrating DCs to sustain T(H)17 responses. This activity of p38α was conserved in mouse and human DCs and was dynamically regulated by pattern recognition and fungal infection. Our results identify p38α signaling as a central pathway for the integration of instructive signals in DCs for T(H)17 differentiation and inflammation.

Indexed as

AnimalsCytokinesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalGene DeletionHumansLymphocyte ActivationMacrophagesMiceMitogen-Activated Protein Kinase 14MycosesReceptors, InterleukinReceptors, Pattern RecognitionTh17 CellsT-LymphocytesCytokinesinterleukin-23 receptor, mouseMitogen-Activated Protein Kinase 14Receptors, InterleukinReceptors, Pattern Recognition

Identifiers

PMID22231518
PMCPMC3262925
OpenAlexW2064539458

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.