Evidence map›Paper›PMID 17548817›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Central histamine H3 receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS.

Cory Teuscher, Meena Subramanian, Rajkumar Noubade, Jian Feng Gao, Halina Offner, James F Zachary, Elizabeth P Blankenhorn

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Pathophysiological role of histamine signaling and its implications in glioblastoma.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
  5. AR71, Histamine HInternational journal of molecular sciences · 2024
    Article
  6. Article
  7. Review
  8. Seasonal Changes in Serum Metabolites in Multiple Sclerosis Relapse.International journal of molecular sciences · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Histamine and histidine decarboxylase: Immunomodulatory functions and regulatory mechanisms.Genes to cells : devoted to molecular & cellular mechanisms · 2020
    Review
  18. Article
  19. Histamine receptor agonist alleviates severe cardiorenal damages by eliciting anti-inflammatory programming.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  20. Article
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 4 institutions in 1 country.

Cory TeuscherDepartments of Medicine and Pathology, University of Vermont, Burlington, VT 05405, USA. c.teuscher@uvm.edu
Meena Subramanian
Rajkumar Noubade
Jian Feng Gao
Halina Offner
James F Zachary
Elizabeth P Blankenhorn
University of Vermont · USDrexel University · USOregon Health & Science University · USUniversity of Illinois Urbana-Champaign · US

Funding

Synovial V delta 1 cells kill Th2 cellsP01AI045666 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI BUDD, RALPH C · 1999 to 2010
$12.5M
Susceptibilty and Resistance Loci in Mouse EAER01NS036526 · NINDS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TEUSCHER, CORY · 1996 to 2008
$4.4M
AUTOIMMUNE DISEASE AND NEONATAL TOLERANCER01AI041747 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TEUSCHER, CORY · 1997 to 2009
$1.9M
Genetics of Suscptibility to Anthrax Toxin in vivoR01AI058052 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2004 to 2008
$1.8M
NIAID NIH HHS AI 041747NIAID NIH HHS AI 045666NIAID NIH HHS AI 058052NIAID NIH HHS P01 AI045666NIAID NIH HHS R01 AI041747NIAID NIH HHS R01 AI058052NINDS NIH HHS NS 036526NINDS NIH HHS R01 NS036526
6 · The paper itself

Abstract

Histamine (HA), a biogenic amine with a broad spectrum of activities in both physiological and pathological settings, plays a key regulatory role in experimental allergic encephalomyelitis, the autoimmune model of multiple sclerosis. HA exerts its effect through four G protein-coupled receptors designated HA receptor H1, H2, H3, and H4. We report here that, compared with wild-type animals, mice with a disrupted HA H3 receptor (H3RKO), the expression of which is normally confined to cells of the nervous system, develop more severe disease and neuroinflammation. We show that this effect is associated with dysregulation of blood-brain barrier permeability and increased expression of MIP-2, IP-10, and CXCR3 by peripheral T cells. Our data suggest that pharmacological targeting of the H3R may be useful in preventing the development and formation of new lesions in multiple sclerosis, thereby significantly limiting the progression of the disease.

Indexed as

Signal TransductionAnimalsCentral Nervous SystemDisease SusceptibilityEncephalomyelitis, Autoimmune, ExperimentalMiceMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutModels, ImmunologicalReceptors, Histamine H3Receptors, Histamine H3

Identifiers

PMID17548817
PMCPMC1891222
OpenAlexW2129535012

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.