Evidence map›Paper›PMID 37120813›Full record

ArticleCell reports2023

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts.

Anna Di Nardo, Yu-Ling Chang, Shahrzad Alimohammadi, Kana Masuda-Kuroki, Zhenping Wang, Krishna Sriram, Paul A Insel

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Anna Di NardoDepartment of Dermatology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA. Electronic address: adinardo@ucsd.edu.
Yu-Ling ChangDepartment of Dermatology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Shahrzad AlimohammadiDepartment of Dermatology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Kana Masuda-KurokiDepartment of Dermatology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Zhenping WangDepartment of Dermatology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Krishna SriramDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA; Department of Medicine, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Paul A InselDepartment of Pharmacology, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA; Department of Medicine, School of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
University of California San Diego · US

Funding

Mast cells in skin innate immune defenseR01AI093957 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DI NARDO, ANNA · 2011 to 2023
$4.6M
Illumina NovaSeq 6000 Sequencing SystemS10OD026929 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JEPSEN, KRISTEN LYNN · 2019 to 2019
$600k
NIAID NIH HHS R01 AI093957NIH HHS S10 OD026929
6 · The paper itself

Abstract

Activation and degranulation of mast cells (MCs) is an essential aspect of innate and adaptive immunity. Skin MCs, the most exposed to the external environment, are at risk of quickly degranulating with potentially severe consequences. Here, we define how MCs assume a tolerant phenotype via crosstalk with dermal fibroblasts (dFBs) and how this phenotype reduces unnecessary inflammation when in contact with beneficial commensal bacteria. We explore the interaction of human MCs (HMCs) and dFBs in the human skin microenvironment and test how this interaction controls MC inflammatory response by inhibiting the nuclear factor κB (NF-κB) pathway. We show that the extracellular matrix hyaluronic acid, as the activator of the regulatory zinc finger (de)ubiquitinating enzyme A20/tumor necrosis factor α-induced protein 3 (TNFAIP3), is responsible for the reduced HMC response to commensal bacteria. The role of hyaluronic acid as an anti-inflammatory ligand on MCs opens new avenues for the potential treatment of inflammatory and allergic disorders.

Indexed as

Hyaluronic AcidMast CellsBacteriaFibroblastsHumansSkinHyaluronic Acidcommensal bacteriaCP: ImmunologyCP: Microbiologyhuman dermal fibroblastshyaluronic acidmast cellsNF–κBTLR2TNFAIP3

Identifiers

PMID37120813
PMCPMC10290424
OpenAlexW4367302280

What OpenQuestion holds

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LicenceCC BY
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.