Evidence map›Paper›PMID 16314476›Full record

ArticleThe American journal of pathology2005

Massive apoptosis in lymphoid organs in animal models for primary and secondary progressive multiple sclerosis.

Ikuo Tsunoda, Jane E Libbey, Li-Qing Kuang, Emily Jane Terry, Robert S Fujinami

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Gas6/TAM System and Multiple Sclerosis.International journal of molecular sciences · 2016
    Review
  8. Article
  9. Article
  10. Article
  11. Diazoxide attenuates autoimmune encephalomyelitis and modulates lymphocyte proliferation and dendritic cell functionality.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Ikuo TsunodaDepartment of Neurology, University of Utah School of Medicine, Salt Lake City, 84132-2305, USA.
Jane E Libbey
Li-Qing Kuang
Emily Jane Terry
Robert S Fujinami
University of Utah · US

Funding

Immunologic Factors In Progressive Autoimmune DiseaseR01NS040350 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2002 to 2005
$998k
NINDS NIH HHS 5R01NS40350NINDS NIH HHS R01 NS040350
6 · The paper itself

Abstract

The mechanism(s) responsible for generating the different forms of multiple sclerosis, primary progressive (PP) and secondary progressive (SP) versus relapsing-remitting (RR), is not well understood. Using myelin oligodendrocyte glycoprotein (MOG)(92-106), we have established animal models that mimic the different types of multiple sclerosis. A.SW mice develop PP or SP-experimental allergic encephalomyelitis (EAE) with large areas of demyelination and high titers of MOG antibody whereas SJL/J mice develop RR-EAE with perivascular T cells and mild demyelination. In A.SW progressive EAE, we found atrophy of the thymus, spleen, and lymph nodes with depletion of T and B cells and massive apoptosis, as demonstrated by immunohistochemistry, terminal dUTP nick-end labeling, and DNA agarose gel electrophoresis. To test whether lymphoid apoptosis itself contributes to disease progression, we injected SJL/J mice with apoptotic thymocytes. Injection of apoptotic cells resulted in greater than 20% of mice developing SP-EAE with ataxia. SJL/J mice with SP-EAE had large areas of demyelination, high MOG antibody titers and atrophic lymphoid organs. Spleen cells from mice with progressive EAE produced less interferon-gamma than those from RR-EAE when stimulated with mitogen. We suggest that induction of lymphoid apoptosis alters the balance of Th1 versus Th2 immune responses and increases MOG antibody production, leading to exacerbation of demyelination and subsequent disease progression.

Indexed as

AnimalsApoptosisB-LymphocytesCytokinesDisease Models, AnimalDisease ProgressionDNA FragmentationElectrophoresis, Agar GelEncephalomyelitis, Autoimmune, ExperimentalFemaleLymph NodesLymphocytesMiceMice, Inbred StrainsMultiple SclerosisRecurrenceCytokines

Identifiers

PMID16314476
PMCPMC1613181
OpenAlexW1964421053

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.