Evidence map›Paper›PMID 18171609›Full record

ArticleBrain, behavior, and immunity2008

The diminishment of experimental autoimmune encephalomyelitis (EAE) by neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH) therapy.

Andrew W Taylor, Nobuyoshi Kitaichi

Abstract readComparative Study
In one paragraph

Article in Brain, behavior, and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Identification and protective role of CD34Histochemistry and cell biology · 2023
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  15. How type I interferons work in multiple sclerosis and other diseases: some unexpected mechanisms.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
  16. Article
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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

2 authors at 1 institution in 1 country.

Andrew W TaylorSchepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA. andrew.taylor@schepens.harvard.edu
Nobuyoshi Kitaichi
Smith-Kettlewell Eye Research Institute · US

Funding

Neuroimmunomodulation within the eyeR01EY010752 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI TAYLOR, ANDREW W · 2002 to 2011
$4.2M
NEI NIH HHS R01 EY010752
6 · The paper itself

Abstract

The neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH) plays an important role in immune privilege by its suppression of inflammation, and its induction of regulatory T cells. This finding led us to test the possibility that we can use alpha-MSH to suppress autoimmune diseases, and promote re-establishment of immune tolerance to autoantigens. To test this possibility, SJL mice with experimental autoimmune encephalomyelitis (EAE) were injected with alpha-MSH at the first signs of paralysis. The alpha-MSH-treated mice in comparison with untreated EAE mice had a profound diminishment in the severity and tempo of EAE. The spleen cells in alpha-MSH-treated EAE produced TGF-beta in response to PLP-antigen stimulation in contrast to untreated mice spleen cells that produced IFN-gamma. When the alpha-MSH-treated EAE mice were reimmunized there was a delay of a week before the second episode of EAE. Although this delay maybe because of the induction of TGF-beta-producing spleen cells by the alpha-MSH-treatment, it was not adequate to suppress IFN-gamma-production by PLP-antigen stimulated spleen cells from untreated mice, nor able to suppress the eventual second episode of EAE. Therefore, the injection of alpha-MSH at the onset of paralysis is extremely effective in diminishing the severity and tempo of EAE, and the subsequent induction of potential PLP-specific Treg cells suggests that an alpha-MSH therapy could be attempted as part of a therapeutic regiment to impose immunoregulation and immunosuppression on an autoimmune disease of the central nervous system.

Indexed as

alpha-MSHAnimalsAutoantigensAutoimmune DiseasesCells, CulturedCentral Nervous SystemDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayHumansImmune ToleranceInflammationInjections, SubcutaneousInterferon-gammaLymphocyte ActivationMicealpha-MSHAutoantigensInterferon-gammainterferon-gamma (95-133)Peptide FragmentsProteolipidsTransforming Growth Factor beta

Identifiers

PMID18171609
PMCPMC3337335
OpenAlexW1980897591

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.