Evidence map›Paper›PMID 25194146›Full record

ArticleInternational immunology2015

In vivo anti-LAP mAb enhances IL-17/IFN-γ responses and abrogates anti-CD3-induced oral tolerance.

Andre P da Cunha, Henry Y Wu, Rafael M Rezende, Tyler Vandeventer, Howard L Weiner

Open access · bronzeAbstract read
In one paragraph

Article in International immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. γδ T Cell-Secreted XCL1 Mediates Anti-CD3-Induced Oral Tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  8. LAPJournal of virology · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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 3 institutions in 1 country.

Andre P da CunhaEvergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USA.
Henry Y WuNovartis Institutes for Biomedical Research, Cambridge, MA 02139, USA.
Rafael M RezendeEvergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Tyler VandeventerEvergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Howard L WeinerEvergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA The Partners Multiple Sclerosis Center, 1 Brookline Place, Brookline, MA 02445, USA hweiner@rics.bwh.harvard.edu.
Brigham and Women's Hospital · USHarvard University · USNovartis (United States) · US

Funding

MECHANISMS OF THE INDUCTION OF ORAL TOLERANCER01AI043458 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 1998 to 2015
$5.0M
NIAID NIH HHS R01 AI043458NIAID NIH HHS R01 AI43458
6 · The paper itself

Abstract

Regulatory T cells (Tregs) play a critical role in the maintenance of immunological tolerance. The best-characterized Tregs are those expressing the transcription factor Foxp3 and in vivo modulation of Foxp3 Tregs has been employed to study their role in immune homeostasis. Latency-associated peptide (LAP) is a membrane-bound TGF-β complex that has also been shown to play a role in Treg function and oral tolerance. We developed a novel anti-mouse LAP mAb that allowed us to investigate the effect of targeting LAP in vivo on immune function and on anti-CD3-induced oral tolerance. We found that in vivo anti-LAP mAb administration led to a decrease in the number of CD4+LAP+ Tregs in spleen and lymph nodes without affecting CD4+Foxp3+ Tregs. Spleen cells from anti-LAP-injected mice proliferated more in vitro and produced increased amounts of IL-2, IL-17 and IFN-γ. Moreover, injection of anti-LAP antibody abrogated the protective effect of oral anti-CD3 on experimental autoimmune encephalomyelitis (EAE). Finally, in vivo anti-LAP administration prior to myelin oligodendrocyte glycoprotein immunization resulted in severe EAE in the absence of pertussis toxin, which is used for EAE induction. Our findings demonstrate the importance of CD4+LAP+ T cells in the control of immune homeostasis and autoimmunity and provides a new tool for the in vivo investigation of murine LAP+ Tregs on immune function.

Indexed as

AnimalsAntibodies, Monoclonal, Murine-DerivedCD3 ComplexEncephalomyelitis, Autoimmune, ExperimentalImmune ToleranceInterferon-gammaInterleukin-17MiceMice, KnockoutPeptidesT-Lymphocytes, RegulatoryAntibodies, Monoclonal, Murine-DerivedCD3 ComplexInterferon-gammaInterleukin-17Peptidesexperimental autoimmune encephalomyelitisinflammationlatency-associated peptideregulatory T cellsTGF-beta

Identifiers

PMID25194146
PMCPMC4303004
OpenAlexW2099098671

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.