Evidence map›Paper›PMID 30195028›Full record

ArticleBrain, behavior, and immunity2018

The β2-adrenergic receptor controls inflammation by driving rapid IL-10 secretion.

Didem Ağaç, Leonardo D Estrada, Robert Maples, Lora V Hooper, J David Farrar

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

126 citing papers in PubMed, 194 citations in OpenAlex.

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  6. Neuroimmune interactions in cardiovascular homeostasis and disease.American journal of physiology. Cell physiology · 2026
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66 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

5 authors at 3 institutions in 1 country.

Didem AğaçDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, United States.
Leonardo D EstradaDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, United States.
Robert MaplesDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, United States.
Lora V HooperDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, United States; Howard Hughes Medical Institute, United States.
J David FarrarDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, United States. Electronic address: david.farrar@utsouthwestern.edu.
Southwestern Medical CenterHoward Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Microbial Regulation of Retinol Transport and its Role in Intestinal ImmunityR01DK070855 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI LORA V HOOPER · 2005 to 2026
$7.9M
INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
DIVISION OF CELL &MOLECULAR BIOLOGY TRAINING PROGRAMT32GM008203 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI COBB, MELANIE H. · 1987 to 2018
$7.0M
Type I Interferon-Regulated T Helper DevelopmentR01AI056222 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI FARRAR, JOHN DAVID · 2005 to 2014
$3.8M
Sympathetic neural control of T cell functionR56AI125545 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI FARRAR, JOHN DAVID · 2016 to 2016
$393k
NIAID NIH HHS R01 AI056222NIAID NIH HHS R56 AI125545NIAID NIH HHS T32 AI005284NIDDK NIH HHS R01 DK070855NIGMS NIH HHS T32 GM008203
6 · The paper itself

Abstract

The mammalian nervous system communicates important information about the environment to the immune system, but the underlying mechanisms are largely unknown. Secondary lymphoid organs are highly innervated by sympathetic neurons that secrete norepinephrine (NE) as the primary neurotransmitter. Immune cells express adrenergic receptors, enabling the sympathetic nervous system to directly control immune function. NE is a potent immunosuppressive factor and markedly inhibits TNF-α secretion from innate cells in response to lipopolysaccharide (LPS). In this study, we demonstrate that NE blocks the secretion of a variety of proinflammatory cytokines by rapidly inducing IL-10 secretion from innate cells in response to multiple Toll-like receptor (TLR) signals. NE mediated these effects exclusively through the β2-adrenergic receptor (ADRB2). Consequently, Adrb2

Indexed as

AnimalsCytokinesImmune SystemInflammationInterleukin-10Interleukin-6LipopolysaccharidesMiceMice, Inbred BALB CMice, Inbred C57BLNorepinephrineReceptors, Adrenergic, beta-2Signal TransductionSympathetic Nervous SystemToll-Like ReceptorsTumor Necrosis Factor-alphaCytokinesInterleukin-10Interleukin-6LipopolysaccharidesNorepinephrineReceptors, Adrenergic, beta-2Toll-Like ReceptorsTumor Necrosis Factor-alphaAdrenergic receptorInflammationInterleukin-10MacrophageNorepinephrineSepsis

Identifiers

PMID30195028
PMCPMC6289674
OpenAlexW2889788554

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.