Evidence map›Paper›PMID 22934095›Full record

ArticleFrontiers in immunology2012

Cytokine-neuroantigen fusion proteins as a new class of tolerogenic, therapeutic vaccines for treatment of inflammatory demyelinating disease in rodent models of multiple sclerosis.

Mark D Mannie, J Lori Blanchfield, S M Touhidul Islam, Derek J Abbott

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  17. Tolerogenic vaccines for Multiple sclerosis.Human vaccines & immunotherapeutics · 2013
    Article
  18. Immunity and inflammation in neurodegenerative diseases.American journal of neurodegenerative disease · 2013
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Mark D MannieDepartment of Microbiology and Immunology, East Carolina University Greenville, NC, USA.
J Lori Blanchfield
S M Touhidul Islam
Derek J Abbott
East Carolina University · USEmory University · US

Funding

Interferons as adjuvants for tolerogenic vaccinesR01NS072150 · NINDS · EAST CAROLINA UNIVERSITY · PI MANNIE, MARK D. · 2011 to 2015
$1.5M
Therapeutic vaccines for treatment of experimental autoimmune encephalomyelitis (R15NS075830 · NINDS · EAST CAROLINA UNIVERSITY · PI MANNIE, MARK D. · 2011 to 2011
$429k
NINDS NIH HHS R01 NS072150NINDS NIH HHS R15 NS075830
6 · The paper itself

Abstract

Myelin-specific induction of tolerance represents a promising means to modify the course of autoimmune inflammatory demyelinating diseases such as multiple sclerosis (MS). Our laboratory has focused on a novel preclinical strategy for the induction of tolerance to the major encephalitogenic epitopes of myelin that cause experimental autoimmune encephalomyelitis (EAE) in rats and mice. This novel approach is based on the use of cytokine-NAg (neuroantigen) fusion proteins comprised of the native cytokine fused either with or without a linker to a NAg domain. Several single-chain cytokine-NAg fusion proteins were tested including GMCSF-NAg, IFNbeta-NAg, NAgIL16, and IL2-NAg. These cytokine-NAg vaccines were tolerogenic, therapeutic vaccines that had tolerogenic activity when given as pre-treatments before encephalitogenic immunization and also were effective as therapeutic interventions during the effector phase of EAE. The rank order of inhibitory activity was as follows: GMCSF-NAg, IFNbeta-NAg > NAgIL16 > IL2-NAg > MCSF-NAg, IL4-NAg, IL-13-NAg, IL1RA-NAg, and NAg. Several cytokine-NAg fusion proteins exhibited antigen-targeting activity. High affinity binding of the cytokine domain to specific cytokine receptors on particular subsets of APC resulted in the concentrated uptake of the NAg domain by those APC which in turn facilitated the enhanced processing and presentation of the NAg domain on cell surface MHC class II glycoproteins. For most cytokine-NAg vaccines, the covalent linkage of the cytokine domain and NAg domain was required for inhibition of EAE, thereby indicating that antigenic targeting of the NAg domain to APC was also required in vivo for tolerogenic activity. Overall, these studies introduced a new concept of cytokine-NAg fusion proteins as a means to induce tolerance and to inhibit the effector phase of autoimmune disease. The approach has broad application for suppressive vaccination as a therapy for autoimmune diseases such as MS.

Indexed as

autoimmune demyelinationcytokine-neuroantigen fusion proteinexperimental autoimmune encephalomyelitisgranulocyte-macrophage colony-stimulating factorimmunological toleranceinterferon-betamultiple sclerosistolerogenic therapeutic vaccine

Identifiers

PMID22934095
PMCPMC3422719
OpenAlexW2132683405

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.