Evidence map›Paper›PMID 19050296›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Targeting of myelin protein zero in a spontaneous autoimmune polyneuropathy.

Hye-Jung Kim, Cha-Gyun Jung, Mark A Jensen, Danuta Dukala, Betty Soliven

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Immune-Mediated Neuropathies: Pathophysiology and Management.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Novel pathomechanisms in inflammatory neuropathies.Journal of neuroinflammation · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. Impaired dendritic cell function in a spontaneous autoimmune polyneuropathy.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  15. VIP-expressing dendritic cells protect against spontaneous autoimmune peripheral polyneuropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 1 institution in 1 country.

Hye-Jung KimDepartment of Neurology, The University of Chicago, Chicago, IL 60637, USA.
Cha-Gyun Jung
Mark A Jensen
Danuta Dukala
Betty Soliven
University of Chicago · US

Funding

Novel therapeutic targets in inflammatory neuropathiesR21NS049014 · NINDS · UNIVERSITY OF CHICAGO · PI SOLIVEN, BETTY C · 2005 to 2006
$349k
NINDS NIH HHS R21 NS049014
6 · The paper itself

Abstract

Elimination of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease chronic inflammatory demyelinating polyneuropathy (CIDP). In this study, we examined the immunopathogenic mechanisms in this model, including identification of SAP Ags. We found that B7-2-deficient NOD mice exhibit changes in cytokine and chemokine gene expression in spleens over time. There was an increase in IL-17 and a decrease in IL-10 transcript levels at 4 mo (preclinical phase), whereas IFN-gamma expression peaked at 8 mo (clinical phase). There was also an increase in transcript levels of Th1 cytokines, CXCL10, and RANTES in sciatic nerves of mice that developed SAP. Splenocytes from SAP mice exhibited proliferative and Th1 cytokine responses to myelin P0 (180-199), but not to other P0 peptides or P2 (53-78). Adoptive transfer of P0-reactive T cells generated from SAP mice induced neuropathy in four of six NOD.SCID mice. Data from i.v. tolerance studies indicate that myelin P0 is one of the autoantigens targeted by T cells in SAP in this model. The expression of P0 by peri-islet Schwann cells provides a potential mechanism linking islet autoimmunity and inflammatory neuropathy.

Indexed as

Amino Acid SequenceAnimalsB7-2 AntigenCell LineCells, CulturedFemaleImmune ToleranceMiceMice, Inbred NODMice, KnockoutMice, SCIDMolecular Sequence DataMyelin P0 ProteinPolyendocrinopathies, AutoimmuneRatsSciatic NerveB7-2 AntigenCd86 protein, mouseMyelin P0 Protein

Identifiers

PMID19050296
PMCPMC2745060
OpenAlexW2095828131

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.