Evidence map›Paper›PMID 9236201›Full record

ArticleThe Journal of experimental medicine1997

Negative signaling pathways of the killer cell inhibitory receptor and Fc gamma RIIb1 require distinct phosphatases.

N Gupta, A M Scharenberg, D N Burshtyn, N Wagtmann, M N Lioubin, L R Rohrschneider, J P Kinet, E O Long

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 92 citations in OpenAlex.

  1. Licensing Natural Killers for Antiviral Immunity.Pathogens (Basel, Switzerland) · 2021
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. SHP-2 expression negatively regulates NK cell function.Journal of immunology (Baltimore, Md. : 1950) · 2009
    Article
  7. Article
  8. Review
  9. Review
  10. Roles of Fc receptors in autoimmunity.Nature reviews. Immunology · 2002
    Review
  11. Article
  12. Article
  13. Article
  14. DSHP: a "power bar" for sustained immune responses?Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  15. LCK-phosphorylated human killer cell-inhibitory receptors recruit and activate phosphatidylinositol 3-kinase.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  16. Article
  17. Article
  18. Review
  19. 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

8 authors at 1 institution in 1 country.

N GuptaLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, Rockville, Maryland 20852, USA.
A M Scharenberg
D N Burshtyn
N Wagtmann
M N Lioubin
L R Rohrschneider
J P Kinet
E O Long
National Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of natural killer (NK) cells by the killer cell inhibitory receptor (KIR) involves recruitment of the tyrosine phosphatase SHP-1 by KIR and is prevented by expression of a dominant negative SHP-1 mutant. Another inhibitory receptor, the low affinity Fc receptor for immunoglobulin G (IgG) (Fc gamma RIIb1), has been shown to bind SHP-1 when cocross-linked with the antigen receptor on B cells (BCR). However, coligation of Fc gamma RIIb1 with BCR and with Fc epsilon RI on mast cells leads to recruitment of the inositol 5' phosphatase SHIP and to inhibition of mast cells from SHP-1-deficient mice. In this study, we evaluated the ability of these two inhibitory receptors to block target cell lysis by NK cells, and the contribution of SHP-1 and SHIP to inhibition. Recombinant vaccinia viruses encoding chimeric receptors and dominant negative mutants of SHP-1 and SHIP were used for expression in mouse and human NK cells. When the KIR cytoplasmic tail was replaced by that of Fc gamma RIIb1, recognition of HLA class I on target cells by the extracellular domain resulted in inhibition. A dominant negative mutant of SHP-1 reverted the inhibition mediated by the KIR cytoplasmic tail but not that mediated by Fc gamma RIIb1. In contrast, a dominant negative mutant of SHIP reverted only the inhibition mediated by the Fc gamma RIIb1 tail, providing functional evidence that SHIP plays a role in the Fc gamma RIIb1-mediated negative signal. These data demonstrate that inhibition of NK cells by KIR involves primarily the tyrosine phosphatase SHP-1, whereas inhibition mediated by Fc gamma RIIb1 requires the inositol phosphatase SHIP.

Indexed as

AnimalsCell LineCytotoxicity, ImmunologicHumansKiller Cells, NaturalMiceMice, Inbred C57BLPhosphoric Monoester HydrolasesProtein Tyrosine PhosphatasesReceptors, IgGReceptors, ImmunologicRecombinant Fusion ProteinsSignal Transductionmyo-inositol-1 (or 4)-monophosphatasePhosphoric Monoester HydrolasesProtein Tyrosine PhosphatasesReceptors, IgGReceptors, ImmunologicRecombinant Fusion Proteins

Identifiers

PMID9236201
PMCPMC2199004
OpenAlexW2017355451

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.