Evidence map›Paper›PMID 19841172›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Analysis of the role of tripeptidyl peptidase II in MHC class I antigen presentation in vivo.

Masahiro Kawahara, Ian A York, Arron Hearn, Diego Farfan, Kenneth L Rock

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Proteostasis in T cell aging.Seminars in immunology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Sequence-specific alterations of epitope production by HIV protease inhibitors.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
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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 2 institutions in 1 country.

Masahiro KawaharaDepartment of Pathology, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Ian A York
Arron Hearn
Diego Farfan
Kenneth L Rock
University of Massachusetts Chan Medical School · USMichigan State University · US

Funding

IMMUNOLOGY OF MHC RESTRICTION OF T CELLSR01AI020248 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ROCK, KENNETH L · 1985 to 2013
$2.0M
NIAID NIH HHS R01 AI020248NIDDK NIH HHS DK42520
6 · The paper itself

Abstract

Previous experiments using enzyme inhibitors and RNA interference in cell lysates and cultured cells have suggested that tripeptidyl peptidase II (TPPII) plays a role in creating and destroying MHC class I-presented peptides. However, its precise contribution to these processes has been controversial. To elucidate the importance of TPPII in MHC class I Ag presentation, we analyzed TPPII-deficient gene-trapped mice and cell lines from these animals. In these mice, the expression level of TPPII was reduced by >90% compared with wild-type mice. Thymocytes from TPPII gene-trapped mice displayed more MHC class I on the cell surface, suggesting that TPPII normally limits Ag presentation by destroying peptides overall. TPPII gene-trapped mice responded as well as did wild-type mice to four epitopes from lymphocytic choriomeningitis virus. The processing and presentation of peptide precursors with long N-terminal extensions in TPPII gene-trapped embryonic fibroblasts was modestly reduced, but in vivo immunization with recombinant lentiviral or vaccinia virus vectors revealed that such peptide precursors induced an equivalent CD8 T cell response in wild-type and TPPII-deficient mice. These data indicate that while TPPII contributes to the trimming of peptides with very long N-terminal extensions, TPPII is not essential for generating most MHC class I-presented peptides or for stimulating CTL responses to several Ags in vivo.

Indexed as

Antigen PresentationAminopeptidasesAnimalsCD8-Positive T-LymphocytesCytotoxicity, ImmunologicDendritic CellsDipeptidyl-Peptidases and Tripeptidyl-PeptidasesEpitopesFibroblastsGenetic VectorsHistocompatibility Antigens Class IInterferon Type ILymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceOvalbuminAminopeptidasesDipeptidyl-Peptidases and Tripeptidyl-PeptidasesEpitopesHistocompatibility Antigens Class IInterferon Type IOvalbuminPoly I-CRNA, MessengerSerine Endopeptidasestripeptidyl-peptidase 2Ubiquitin

Identifiers

PMID19841172
PMCPMC4314709
OpenAlexW1900063567

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.