Evidence map›Paper›PMID 23365459›Full record

ArticleBlood2013

Neurokinin-1 receptor agonists bias therapeutic dendritic cells to induce type 1 immunity by licensing host dendritic cells to produce IL-12.

Brian M Janelsins, Tina L Sumpter, Olga A Tkacheva, Darling M Rojas-Canales, Geza Erdos, Alicia R Mathers, William J Shufesky, Walter J Storkus, Louis D Falo, Adrian E Morelli and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

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  18. Substance P-Friend or Foe.Journal of clinical medicine · 2022
    Article
  19. Review
  20. Substance P, A Promising Therapeutic Target in Musculoskeletal Disorders.International journal of molecular sciences · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Brian M JanelsinsDepartment of Dermatology, University of Pittsburgh, 200 Lothrop St, Pittsburgh, PA 15213, USA.
Tina L Sumpter
Olga A Tkacheva
Darling M Rojas-Canales
Geza Erdos
Alicia R Mathers
William J Shufesky
Walter J Storkus
Louis D Falo
Adrian E Morelli
Adriana T Larregina
McGowan Institute for Regenerative Medicine · USUPMC Hillman Cancer Center · US

Funding

Therapuetic Immune Targeting of EphA2 Expressed by Melanoma & Its Tumor-AssociateP50CA121973 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KIRKWOOD, JOHN MUNN · 2008 to 2018
$22.9M
Use of Substance P antagonists to regulate the skin immune functionR01AI077511 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LARREGINA, ADRIANA T · 2009 to 2013
$1.8M
NCI NIH HHS P50 CA121973NIAID NIH HHS AI077511NIAID NIH HHS R01 AI077511
6 · The paper itself

Abstract

Substance-P and hemokinin-1 are proinflammatory neuropeptides with potential to promote type 1 immunity through agonistic binding to neurokinin-1 receptor (NK1R). Dendritic cells (DCs) are professional antigen-presenting cells that initiate and regulate the outcome of innate and adaptive immune responses. Immunostimulatory DCs are highly desired for the development of positive immunization techniques. DCs express functional NK1R; however, regardless of their potential DC-stimulatory function, the ability of NK1R agonists to promote immunostimulatory DCs remains unexplored. Here, we demonstrate that NK1R signaling activates therapeutic DCs capable of biasing type 1 immunity by inhibition of interleukin-10 (IL-10) synthesis and secretion, without affecting their low levels of IL-12 production. The potent type 1 effector immune response observed following cutaneous administration of NK1R-signaled DCs required their homing in skin-draining lymph nodes (sDLNs) where they induced inflammation and licensed endogenous-conventional sDLN-resident and -recruited inflammatory DCs to secrete IL-12. Our data demonstrate that NK1R signaling promotes immunostimulatory DCs, and provide relevant insight into the mechanisms used by neuromediators to regulate innate and adaptive immune responses.

Indexed as

AnimalsBone Marrow CellsCells, CulturedCyclic AMP Response Element-Binding ProteinDendritic CellsFlow CytometryImmunity, CellularImmunizationImmunophenotypingInterleukin-10Interleukin-12Mechanistic Target of Rapamycin Complex 2MiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinInterleukin-10Interleukin-12Mechanistic Target of Rapamycin Complex 2Multiprotein ComplexesReceptors, Neurokinin-1TOR Serine-Threonine Kinases

Identifiers

PMID23365459
PMCPMC3624938
OpenAlexW2078515335

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.