Evidence map›Paper›PMID 25422496›Full record

ArticleThe Journal of experimental medicine2014

Control of lymphocyte egress from lymph nodes through β2-adrenergic receptors.

Akiko Nakai, Yuki Hayano, Fumika Furuta, Masaki Noda, Kazuhiro Suzuki

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed
8.0field-weighted citation impact, top 1% 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

164 citing papers in PubMed, 268 citations in OpenAlex.

  1. Article
  2. Review
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  5. Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  6. Review
  7. Neuroimmune interactions in cardiovascular homeostasis and disease.American journal of physiology. Cell physiology · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Cancer Neuroscience: Decoding Neural Circuitry in Tumor Evolution for Targeted Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  18. Article
  19. Article
  20. The βScience advances · 2025
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Akiko NakaiWPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
Yuki HayanoWPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
Fumika FurutaWPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
Masaki NodaDepartment of Molecular Pharmacology, Medical Research Institute, Global Center of Excellence Program, and Department of Maxillofacial Orthognathics, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Kazuhiro SuzukiWPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan ksuzuki@ifrec.osaka-u.ac.jp.
Osaka University · JPJapan Science and Technology Agency · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphocyte recirculation through secondary lymphoid organs is essential for immunosurveillance and lymphocyte effector functions. Here, we show that signals through β2-adrenergic receptors (β2ARs) expressed on lymphocytes are involved in the control of lymphocyte dynamics by altering the responsiveness of chemoattractant receptors. Agonist stimulation of lymphocyte β2ARs inhibited egress of lymphocytes from lymph nodes (LNs) and rapidly produced lymphopenia in mice. Physiological inputs from adrenergic nerves contributed to retention of lymphocytes within LNs and homeostasis of their distribution among lymphoid tissues. β2ARs physically interacted with CCR7 and CXCR4, chemokine receptors promoting lymphocyte retention in LNs. Activation of β2ARs enhanced retention-promoting signals through CCR7 and CXCR4, and consequently inhibited lymphocyte egress from LNs. In models of T cell-mediated inflammatory diseases, β2AR-mediated signals inhibited LN egress of antigen-primed T cells and reduced their recruitment into peripheral tissues. Thus, this study reveals a novel mechanism for controlling lymphocyte trafficking and provides additional insights into immune regulation by the nervous system.

Indexed as

AnimalsAntigensInflammationLymph NodesLymphocytesLymphopeniaMice, Inbred C57BLProtein BindingReceptors, Adrenergic, beta-2Receptors, CCR7Receptors, CXCR4Signal TransductionAntigensReceptors, Adrenergic, beta-2Receptors, CCR7Receptors, CXCR4

Identifiers

PMID25422496
PMCPMC4267238
OpenAlexW2171912692

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.