Evidence map›Paper›PMID 23239102›Full record

ReviewMedicinal research reviews2014

Raising the roof: the preferential pharmacological stimulation of Th1 and th2 responses mediated by NKT cells.

James E East, Andrew J Kennedy, Tonya J Webb

Open access · greenAbstract readReview
In one paragraph

Review in Medicinal research reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Novel lipid antigens for NKT cells in cancer.Frontiers in immunology · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. 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

3 authors at 2 institutions in 1 country.

James E EastDepartment of Microbiology and Immunology, The Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201.
Andrew J Kennedy
Tonya J Webb
University of Maryland, Baltimore · USUniversity of Virginia · US

Funding

UNIVERSITY OF MARYLAND GREENEBAUM CANCER CENTERSUPPORT GRANTP30CA134274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI FEYRUZ VIRGILIA RASSOOL · 2008 to 2026
$51.0M
Training Grant in Cancer BiologyT32CA154274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI Toni M Antalis, CURT I CIVIN · 2011 to 2026
$6.8M
aAPC-Mediated NKT cell Modulation to Enhance Cancer ImmunotherapyK01CA131487 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2008 to 2012
$584k
Restoring NKT cell function: a novel immunotherapeutic strategy for Breast CancerR21CA162273 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2011 to 2012
$367k
Altered cellular bioenergetics influences NKT cell mediated responses to LymphomaR21CA162277 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI WEBB, TONYA J. · 2011 to 2012
$359k
NCI NIH HHS K01 CA131487NCI NIH HHS P30 CA134274NCI NIH HHS R21 CA162273NCI NIH HHS R21 CA162277NCI NIH HHS T32 CA154274
6 · The paper itself

Abstract

Natural killer T (NKT) cells serve as a bridge between the innate and adaptive immune systems, and manipulating their effector functions can have therapeutic significances in the treatment of autoimmunity, transplant biology, infectious disease, and cancer. NKT cells are a subset of T cells that express cell-surface markers characteristic of both natural killer cells and T cells. These unique immunologic cells have been demonstrated to serve as a link between the innate and adaptive immune systems through their potent cytokine production following the recognition of a range of lipid antigens, mediated through presentation of the major histocompatibility complex (MHC) class I like CD1d molecule, in addition to the NKT cell's cytotoxic capabilities upon activation. Although a number of glycolipid antigens have been shown to complex with CD1d molecules, most notably the marine sponge derived glycolipid alpha-galactosylceramide (α-GalCer), there has been debate as to the identity of the endogenous activating lipid presented to the T-cell receptor (TCR) via the CD1d molecule on antigen-presenting cells (APCs). This review aims to survey the use of pharmacological agents and subsequent structure-activity relationships (SAR) that have given insight into the binding interaction of glycolipids with both the CD1d molecules as well as the TCR and the subsequent immunologic response of NKT cells. These studies not only elucidate basic binding interactions but also pave the way for future pharmacological modulation of NKT cell responses.

Indexed as

AnimalsCarbohydrate SequenceGalactosylceramidesGlycolipidsHumansKiller Cells, NaturalMolecular Sequence DataStructure-Activity RelationshipTh1 CellsTh2 Cellsalpha-galactosylceramideGalactosylceramidesGlycolipidsCD1d moleculeslipid antigensNKT cells

Identifiers

PMID23239102
PMCPMC4102678
OpenAlexW1683266792

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.