Evidence map›Paper›PMID 16123219›Full record

ArticleBlood2005

Costimulation of mast cells by 4-1BB, a member of the tumor necrosis factor receptor superfamily, with the high-affinity IgE receptor.

Hajime Nishimoto, Seung-Woo Lee, Hong Hong, Karen G Potter, Mari Maeda-Yamamoto, Tatsuya Kinoshita, Yuko Kawakami, Robert S Mittler, Byoung S Kwon, Carl F Ware and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  16. Article
  17. 4-1BB signaling beyond T cells.Cellular & molecular immunology · 2011
    Review
  18. Article
  19. Review
  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

12 authors at 3 institutions in 2 countries.

Hajime NishimotoDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Dr, San Diego, CA 92121, USA.
Seung-Woo Lee
Hong Hong
Karen G Potter
Mari Maeda-Yamamoto
Tatsuya Kinoshita
Yuko Kawakami
Robert S Mittler
Byoung S Kwon
Carl F Ware
Michael Croft
Toshiaki Kawakami
Institute of Vegetable and Floriculture Science · JPEmory University · USLa Jolla Institute for Immunology · US

Funding

SPHINGOMYELIN SIGNALING PATHWAY IN FAS-INDUCED APOPTOSISP01CA069381 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 1996 to 2009
$16.8M
Lymphotoxin alpha Beta and LIGHT cytokine systemsR37AI033068 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2003 to 2012
$4.2M
The Role of 4-IBB in T Cell and APC InteractionsR01AI042944 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 1998 to 2010
$2.9M
IgE Regulation of Mast Cell Growth and SurvivalR01AI050209 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2002 to 2006
$2.3M
ROLES OF PH DOMAINS IN MAST CELL SIGNAL TRANSDUCTIONR01AI038348 · NIAID · LA JOLLA INST FOR ALLERGY &IMMUNOLGY · PI KAWAKAMI, TOSHIAKI · 1996 to 2005
$1.3M
NCI NIH HHS CA69381NIAID NIH HHS AI38348NIAID NIH HHS AI42944NIAID NIH HHS AI50209NIAID NIH HHS R01 AI038348NIAID NIH HHS R01 AI050209NIAID NIH HHS R37 AI33068
6 · The paper itself

Abstract

Mast cells are the major effector-cell type for immediate hypersensitivity and other forms of allergic reactions. Expression of 4-1BB, a member of the tumor necrosis factor receptor superfamily, is induced at mRNA and protein levels on stimulation through the high-affinity receptor for immunoglobulin E (IgE; FcepsilonRI). In this study, we present evidence that agonistic anti-4-1BB antibodies can enhance FcepsilonRI-induced cytokine production and secretion. Consistent with this, 4-1BB-deficient mast cells exhibit reduced degranulation and cytokine production on FcepsilonRI stimulation. Analysis of 4-1BB ligand (4-1BBL)-deficient cells supported this notion. As a potential mechanism for these defects, we identified a defect in Ca2+ flux induced by FcepsilonRI stimulation. The defective Ca2+ flux could be accounted for by the reduced activity of Lyn/Btk/phospholipase C-gamma2 pathway and constitutive interactions between 4-1BB and Lyn. Therefore, FcepsilonRI-inducible 4-1BB plays a costimulatory function together with FcepsilonRI stimulation.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsAntibodies, MonoclonalAntigens, CDCalciumCell ProliferationCells, CulturedCytokinesGene Expression RegulationMast CellsMiceMice, KnockoutPhospholipase C gammaProtein-Tyrosine KinasesReceptors, IgEReceptors, Nerve Growth FactorAgammaglobulinaemia Tyrosine KinaseAntibodies, MonoclonalAntigens, CDCalciumCytokineslyn protein-tyrosine kinasePhospholipase C gammaProtein-Tyrosine KinasesReceptors, IgEReceptors, Nerve Growth FactorReceptors, Tumor Necrosis FactorRNA, Messengersrc-Family KinasesTnfrsf9 protein, mouseTumor Necrosis Factor Receptor Superfamily, Member 9

Identifiers

PMID16123219
PMCPMC1416206
OpenAlexW2159536303

What OpenQuestion holds

Textmetadata
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.