Evidence map›Paper›PMID 26231120›Full record

ArticleImmunity2015

Protein Tyrosine Phosphatase PTPRS Is an Inhibitory Receptor on Human and Murine Plasmacytoid Dendritic Cells.

Anna Bunin, Vanja Sisirak, Hiyaa S Ghosh, Lucja T Grajkowska, Z Esther Hou, Michelle Miron, Cliff Yang, Michele Ceribelli, Noriko Uetani, Laurence Chaperot and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

45 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

18 authors at 5 institutions in 3 countries.

Anna BuninDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA; Celiac Disease Center, Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA.
Vanja SisirakDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA; Department of Pathology and Department of Medicine, New York University Langone Medical Center, New York, NY 10016, USA.
Hiyaa S GhoshDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA.
Lucja T GrajkowskaDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA; Department of Pathology and Department of Medicine, New York University Langone Medical Center, New York, NY 10016, USA.
Z Esther HouDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA.
Michelle MironDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA.
Cliff YangDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA.
Michele CeribelliLymphoid Malignancy Branch, Center for Cancer Research, National Cancer Institute, Rockville, MD 20852, USA.
Noriko UetaniGoodman Cancer Centre, McGill University, Montreal, Quebec H3A 1A3, Canada.
Laurence ChaperotR&D Laboratory, EFS Rhone-Alpes Grenoble, La Tronche F-38701, France.
Joel PlumasR&D Laboratory, EFS Rhone-Alpes Grenoble, La Tronche F-38701, France.
Wiljan HendriksDepartment of Cell Biology, Radboud University, 6525 GA Nijmegen Medical Center, Nijmegen, The Netherlands.
Michel L TremblayGoodman Cancer Centre, McGill University, Montreal, Quebec H3A 1A3, Canada.
Hans HäckerDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Louis M StaudtLymphoid Malignancy Branch, Center for Cancer Research, National Cancer Institute, Rockville, MD 20852, USA.
Peter H GreenCeliac Disease Center, Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA.
Govind BhagatCeliac Disease Center, Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA.
Boris ReizisDepartment of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA; Department of Pathology and Department of Medicine, New York University Langone Medical Center, New York, NY 10016, USA. Electronic address: boris.reizis@nyumc.org.
Columbia University Irving Medical Center · USMcGill University · CANational Cancer Institute · USRadboud University Nijmegen · NLSt. Jude Children's Research Hospital · US

Funding

CELL, MOLECULAR AND DEVELOPMENTAL BIOLOGY OF CANCERT32CA009503 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GAUTIER, JEAN · 1985 to 2016
$6.8M
Molecular Control of Plasmacytoid Dendritic Cell Development and FunctionR37AI072571 · NIAID · UNIVERSITY OF CHICAGO · PI Boris Reizis · 2018 to 2026
$5.3M
Molecular Control of Plasmacytoid Dendritic Cell Development and FunctionR01AI072571 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI REIZIS, BORIS · 2008 to 2017
$4.1M
Columbia University Graduate Training Program in Microbiology and ImmunologyT32AI106711 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Nicholas Arpaia, Uttiya Basu · 2014 to 2026
$2.1M
NCI NIH HHS CA009503NCI NIH HHS T32 CA009503NIAID NIH HHS R01 AI072571NIAID NIH HHS R37 AI072571NIAID NIH HHS T32 AI106711
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) are primary producers of type I interferon (IFN) in response to viruses. The IFN-producing capacity of pDCs is regulated by specific inhibitory receptors, yet none of the known receptors are conserved in evolution. We report that within the human immune system, receptor protein tyrosine phosphatase sigma (PTPRS) is expressed specifically on pDCs. Surface PTPRS was rapidly downregulated after pDC activation, and only PTPRS(-) pDCs produced IFN-α. Antibody-mediated PTPRS crosslinking inhibited pDC activation, whereas PTPRS knockdown enhanced IFN response in a pDC cell line. Similarly, murine Ptprs and the homologous receptor phosphatase Ptprf were specifically co-expressed in murine pDCs. Haplodeficiency or DC-specific deletion of Ptprs on Ptprf-deficient background were associated with enhanced IFN response of pDCs, leukocyte infiltration in the intestine and mild colitis. Thus, PTPRS represents an evolutionarily conserved pDC-specific inhibitory receptor, and is required to prevent spontaneous IFN production and immune-mediated intestinal inflammation.

Indexed as

AnimalsCell DifferentiationCell MovementCells, CulturedColitisDendritic CellsDisease Models, AnimalHumansInterferon-gammaIntestinesLeukocytesMiceMice, Inbred C57BLMice, KnockoutReceptor-Like Protein Tyrosine Phosphatases, Class 2Interferon-gammaPtprf protein, mousePTPRS protein, humanPtprs protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 2

Identifiers

PMID26231120
PMCPMC4547994
OpenAlexW1501014477

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.