Evidence map›Paper›PMID 22888134›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Myelin basic protein-specific TCR/HLA-DRB5*01:01 transgenic mice support the etiologic role of DRB5*01:01 in multiple sclerosis.

Jacqueline A Quandt, Jaebong Huh, Mirza Baig, Karen Yao, Naoko Ito, Mark Bryant, Kazuyuki Kawamura, Clemencia Pinilla, Henry F McFarland, Roland Martin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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
1.3field-weighted citation impact, top 21% 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, 52 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Increased HLA-DR expression and cortical demyelination in MS links with HLA-DR15.Neurology(R) neuroimmunology & neuroinflammation · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

11 authors at 5 institutions in 1 country.

Jacqueline A QuandtNeuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. jquandt@pathology.ubc.ca
Jaebong Huh
Mirza Baig
Karen Yao
Naoko Ito
Mark Bryant
Kazuyuki Kawamura
Clemencia Pinilla
Henry F McFarland
Roland Martin
Kouichi Ito
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · USEnvironmental and Occupational Health Sciences Institute · USOffice of Research Services · USTorrey Pines Institute For Molecular Studies · US

Funding

Human Keratin (K14)-MBP/MBP-TCR Transgenic Animal ModelR21AI067474 · NIAID · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ITO, KOUICHI · 2008 to 2009
$407k
Intramural NIH HHSNIAID NIH HHS R21 AI067474
6 · The paper itself

Abstract

Genetic susceptibility to multiple sclerosis (MS) has been linked to the HLA-DR15 haplotype consisting of DRB1*15:01(DR2b) and DRB5*01:01(DR2a) alleles. Given almost complete linkage disequilibrium of the two alleles, recent studies suggested differential roles in susceptibility (DR2b) or protection from MS (DR2a). Our objective was to assess the potential contribution of DR2a to disease etiology in MS using a humanized model of autoimmunity. To assess the potential contribution of DR2a to disease etiology, we created DR2a humanized transgenic (Tg) mice and subsequently crossed them to Tg mice expressing TL3A6, an MS patient-derived myelin basic protein 83-99-specific TCR. In TL3A6/DR2a Tg mice, CD4 Tg T cells escape thymic and peripheral deletion and initiate spontaneous experimental autoimmune encephalomyelitis (EAE) at low rates, depending on the level of DR2a expression. The ability to induce active EAE was also increased in animals expressing higher levels of DR2a. Inflammatory infiltrates and neuronal damage were present throughout the spinal cord, consistent with a classical ascending EAE phenotype with minor involvement of the cerebellum, brainstem, and peripheral nerve roots in spontaneous, as well as actively induced, disease. These studies emphasize the pathologic contribution of the DR2a allele to the development of autoimmunity when expressed as the sole MHC class II molecule, as well as strongly argue for DR2a as a contributor to the CNS autoimmunity in MS.

Indexed as

Adoptive TransferAnimalsCD4-Positive T-LymphocytesDisease Models, AnimalEpitopes, T-LymphocyteGenetic Predisposition to DiseaseGranulocyte-Macrophage Colony-Stimulating FactorHLA-DRB5 ChainsHumansMiceMice, KnockoutMice, TransgenicMultiple SclerosisReceptors, Antigen, T-CellTh17 CellsTh1 CellsEpitopes, T-LymphocyteGranulocyte-Macrophage Colony-Stimulating FactorHLA-DRB5 ChainsReceptors, Antigen, T-Cell

Identifiers

PMID22888134
PMCPMC3436970
OpenAlexW2123679223

What OpenQuestion holds

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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.