Evidence map›Paper›PMID 42580342›Full record

ArticleImmunity2026

The genesis of cutaneous neurogenic inflammation is a multi-step process requiring dendritic cell aggregation.

Chien-Sin Chen, Jacob E Gillis, Jonathan A Cohen, Alexandra R Glathar, Yijia Chen, Eric S Weiss, Lindsay M McKendrick, Caitlin O Bacon, Colton J Smith, Nick J Spencer and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Chien-Sin ChenDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Jacob E GillisDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Jonathan A CohenDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Alexandra R GlatharDepartment of Immunology, University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh, Center for Systems Immunology, Pittsburgh, PA, USA; University of Pittsburgh Medical Center, Hillman Cancer Center, Pittsburgh, PA, USA; Tumor Microenvironment Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.
Yijia ChenDepartment of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Eric S WeissDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Lindsay M McKendrickDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA.
Caitlin O BaconDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Colton J SmithDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Nick J SpencerCollege of Medicine and Public Health, Flinders Health and Medical Research Institute, Adelaide, SA, Australia.
Isaac M ChiuDepartment of Immunology, Harvard Medical School, Boston, MA, USA.
Brian M DavisDepartment of Neurobiology, University of Pittsburgh, Pittsburgh, PA, USA.
Tina L SumpterDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Anthony R CilloDepartment of Immunology, University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh, Center for Systems Immunology, Pittsburgh, PA, USA; University of Pittsburgh Medical Center, Hillman Cancer Center, Pittsburgh, PA, USA; Cancer Immunology and Immunotherapy Program, UPMC Hillman Cancer Center, Pittsburgh, PA, USA; Tumor Microenvironment Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.
Amanda C PoholekDepartment of Immunology, University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh, Center for Systems Immunology, Pittsburgh, PA, USA.
Daniel H KaplanDepartment of Dermatology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh, Center for Systems Immunology, Pittsburgh, PA, USA. Electronic address: dankaplan@pitt.edu.

Funding

Autoimmunity and Immunopathology Training ProgramT32AI089443 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHLOMCHIK, MARK J · 2010 to 2024
$6.6M
Immune Functions of Cutaneous NociceptorsR01AR071720 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Daniel H Kaplan · 2017 to 2026
$4.1M
Epidermal Nonpeptidergic Nerves Modulate Cutaneous ImmunityR01AR077341 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALBERS, KATHRYN MARIE, KAPLAN, DANIEL H · 2020 to 2024
$2.7M
NIAID NIH HHS T32 AI089443NIAMS NIH HHS R01 AR071720NIAMS NIH HHS R01 AR077341
6 · The paper itself

Abstract

Cutaneous inflammation involving neuroimmune interactions can be initiated by both neurons and immune cells, making it complicated to parse the mechanisms of neurogenic inflammation. Optogenetic activation of Trpv1-expressing nociceptors drives type-17 inflammation in the absence of other inflammatory triggers. We found that two rounds of nociceptor activation were required for Il23a expression and maximal expression of Il1b and Il6, key drivers of type-17 inflammation. The first round of nociceptor activation triggered transient type 2 dendritic cell (DC2) aggregation that required substance P-Mrgprb2-dependent mast cell activation and mast cell-derived chemokine CCL2. Spatial transcriptomic analysis revealed that DC aggregation allowed the second nociceptor stimulation to efficiently activate DCs via the neuropeptide calcitonin gene-related peptide α (CGRPα). Thus, early neurogenic inflammation is a two-step process: substance P induces Mrgprb2-dependent mast cell activation and formation of DC aggregates that allow for efficient subsequent CGRPα-mediated DC activation. These data reveal a multi-cell, dynamic mechanism underlying neurogenic inflammation.

Indexed as

CCL2CGRPαdendritic cellsmast cellsMrgprB2neurogenic inflammationnociceptorssubstance PTrpv1 neurons

Identifiers

PMID42580342
PMCPMC13580354

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.