Evidence map›Paper›PMID 20404101›Full record

ArticleThe Journal of experimental medicine2010

Co-receptor choice by V alpha14i NKT cells is driven by Th-POK expression rather than avoidance of CD8-mediated negative selection.

Isaac Engel, Kirsten Hammond, Barbara A Sullivan, Xi He, Ichiro Taniuchi, Dietmar Kappes, Mitchell Kronenberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Primordial Cells Bridging the Gap Between Innate and Adaptive Immunity.Advances in experimental medicine and biology · 2025
    Review
  3. Markers and makers of NKT17 cells.Experimental & molecular medicine · 2023
    Review
  4. Article
  5. Article
  6. A humanized mouse model forFrontiers in immunology · 2022
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. A Subset of CD8αβ+ Invariant NKT Cells in a Humanized Mouse Model.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  16. Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. T cell recognition of non-peptidic antigens in infectious diseases.The Indian journal of medical research · 2013
    Review
  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

7 authors at 3 institutions in 2 countries.

Isaac EngelLa Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Kirsten Hammond
Barbara A Sullivan
Xi He
Ichiro Taniuchi
Dietmar Kappes
Mitchell Kronenberg
La Jolla Institute for Immunology · USFox Chase Cancer Center · USRIKEN Center for Integrative Medical Sciences · JP

Funding

Development and Function of NKT CellsR37AI071922 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2006 to 2015
$4.9M
CONTROL OF LINEAGE COMMITMENT IN DEVELOPING THYMOCYTESR01AI042915 · NIAID · RESEARCH INST OF FOX CHASE CAN CTR · PI KAPPES, DIETMAR J · 1999 to 2008
$3.3M
Control of Lineage Commitment in Developing ThymocytesR01CA153260 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI KAPPES, DIETMAR J · 2010 to 2014
$1.9M
NCI NIH HHS R01 CA153260NIAID NIH HHS R01 AI042915NIAID NIH HHS R01 AI42915NIAID NIH HHS R37 AI071922NIAID NIH HHS R37 AI71922
6 · The paper itself

Abstract

Mouse natural killer T (NKT) cells with an invariant V alpha14-J alpha18 rearrangement (V alpha14 invariant [V alpha14i] NKT cells) are either CD4(+)CD8(-) or CD4(-)CD8(-). Because transgenic mice with forced CD8 expression in all T cells exhibited a profound NKT cell deficit, the absence of CD8 has been attributed to negative selection. We now present evidence that CD8 does not serve as a coreceptor for CD1d recognition and that the defect in development in CD8 transgene homozygous mice is the result of a reduction in secondary T cell receptor alpha rearrangements. Thymocytes from mice hemizygous for the CD8 transgene have a less severe rearrangement defect and have functional CD8(+) V alpha14i NKT cells. Furthermore, we demonstrate that the transcription factor Th, Poxviruses and Zinc finger, and Krüppel family (Th-POK) is expressed by V alpha14i NKT cells throughout their differentiation and is necessary both to silence CD8 expression and for the functional maturity of V alpha14i NKT cells. We therefore suggest that Th-POK expression is required for the normal development of V alpha14i NKT cells and that the absence of CD8 expression by these cells is a by-product of such expression, as opposed to the result of negative selection of CD8-expressing V alpha14i NKT cells.

Indexed as

AnimalsAntigens, CD1Antigens, CD1dCD4 AntigensCD8 AntigensCD8-Positive T-LymphocytesGene RearrangementHomozygoteHumansKiller Cells, NaturalLymphocyte ActivationMiceMice, KnockoutMice, TransgenicReceptors, Antigen, T-CellAntigens, CD1Antigens, CD1dCD4 AntigensCD8 AntigensReceptors, Antigen, T-Cell

Identifiers

PMID20404101
PMCPMC2867285
OpenAlexW2110476061

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.