Evidence map›Paper›PMID 21833020›Full record

ArticleThe Journal of investigative dermatology2012

GILT modulates CD4+ T-cell tolerance to the melanocyte differentiation antigen tyrosinase-related protein 1.

Matthew P Rausch, K Taraszka Hastings

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  9. Article
  10. Annals of translational medicine · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. HMGB1 in health and disease.Molecular aspects of medicine · 2014
    Review
  17. Article
  18. Article
  19. Review
  20. Expanding roles for GILT in immunity.Current opinion in immunology · 2013
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Matthew P RauschDepartment of Basic Medical Sciences, College of Medicine Phoenix, University of Arizona, Phoenix, Arizona 85004, USA.
K Taraszka Hastings
University of Arizona · US

Funding

Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
MHC Class II Antigen Processing and Immune Recognition of MelanomaK08AR054388 · NIAMS · UNIVERSITY OF ARIZONA · PI HASTINGS, KAREN TARASZKA · 2007 to 2011
$621k
NCI NIH HHS T32 CA009213NCI NIH HHS T32-CA09213NIAMS NIH HHS K08 AR054388NIAMS NIH HHS K08-AR054388
6 · The paper itself

Abstract

Gamma-IFN-inducible lysosomal thiol reductase (GILT) facilitates major histocompatibility complex class II-restricted processing through endocytic reduction of protein disulfide bonds and is necessary for efficient class II-restricted processing of melanocyte differentiation antigen, tyrosinase-related protein 1 (TRP1). Using class II-restricted, TRP1-specific T-cell receptor transgenic mice, we identify a role, to our knowledge, previously unreported, for GILT in the maintenance of tolerance to TRP1. TRP1-specific thymocytes are centrally deleted in the presence of GILT and TRP1. In contrast, CD4 single-positive thymocytes and peripheral T cells develop in the absence of GILT or TRP1, demonstrating that GILT is required for negative selection of TRP1-specific thymocytes. Although TRP1-specific T cells escape thymic deletion in the absence of GILT, they are tolerant to TRP1 and do not induce vilitigo. TRP1-specific T cells that develop in the absence of GILT have diminished IL-2 and IFN-γ production. Furthermore, GILT-deficient mice have a 4-fold increase in the percentage of TRP1-specific regulatory T (Treg) cells compared with TRP1-deficient mice, and depletion of Treg cells partially restores the ability of GILT-deficient TRP1-specific CD4(+) T cells to induce vitiligo. Thus, GILT has a critical role in regulating CD4(+) T-cell tolerance to an endogenous skin-restricted antigen relevant to controlling autoimmunity and generating effective immunotherapy for melanoma.

Indexed as

Adoptive TransferAnimalsCarcinoma, Squamous CellCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedCytokinesHomeodomain ProteinsImmune ToleranceMelanomaMiceMice, Inbred C57BLMice, TransgenicOxidoreductasesOxidoreductases Acting on Sulfur Group DonorsSkin NeoplasmsCytokinesHomeodomain ProteinsIfi30 protein, mouseOxidoreductasesOxidoreductases Acting on Sulfur Group DonorsRAG-1 proteintyrosinase-related protein-1

Identifiers

PMID21833020
PMCPMC3217059
OpenAlexW2044934278

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.