Evidence map›Paper›PMID 12782712›Full record

ArticleThe Journal of experimental medicine2003

Preferential signaling and induction of allergy-promoting lymphokines upon weak stimulation of the high affinity IgE receptor on mast cells.

Claudia Gonzalez-Espinosa, Sandra Odom, Ana Olivera, J Peyton Hobson, Maria Eugenia Cid Martinez, Antonio Oliveira-Dos-Santos, Lillian Barra, Sarah Spiegel, Josef M Penninger, Juan Rivera

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 144 citations in OpenAlex.

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  12. Tetraspanins in the regulation of mast cell function.Medical microbiology and immunology · 2020
    Review
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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

10 authors at 6 institutions in 4 countries.

Claudia Gonzalez-EspinosaMolecular Inflammation Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Sandra Odom
Ana Olivera
J Peyton Hobson
Maria Eugenia Cid Martinez
Antonio Oliveira-Dos-Santos
Lillian Barra
Sarah Spiegel
Josef M Penninger
Juan Rivera
Center for Research and Advanced Studies of the National Polytechnic Institute · MXNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USUniversity Health Network · CAVirginia Commonwealth University Medical Center · USAustrian Academy of Sciences · ATNational Institutes of Health · US

Funding

Intracellular Signaling By The Cell Surface Receptor For IgEZIAAR041101 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RIVERA, JUAN · 2009 to 2013
$4.8M
INTRACELLULAR SIGNALING BY THE CELL SURFACE RECEPTOR FOR IGEZ01AR041101 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RIVERA, JUAN · 1995 to 2008
$2.7M
6 · The paper itself

Abstract

Mast cell degranulation and de novo cytokine production is a consequence of antigen-aggregation of the immunoglobulin E (IgE)-occupied high affinity receptor for IgE (Fc epsilon RI). Herein, we report that lymphokines that promote allergic inflammation, like MCP-1, were potently induced at low antigen (Ag) concentrations or at low receptor occupancy with IgE whereas some that down-regulate this response, like interleukin (IL)-10, required high receptor occupancy. Weak stimulation of mast cells caused minimal degranulation whereas a half-maximal secretory response was observed for chemokines and, with the exception of TNF-alpha, a weaker cytokine secretory response was observed. The medium from weakly stimulated mast cells elicited a monocyte/macrophage chemotactic response similar to that observed at high receptor occupancy. Weak stimulation also favored the phosphorylation of Gab2 and p38MAPK, while LAT and ERK2 phosphorylation was induced by a stronger stimulus. Gab2-deficient mast cells were severely impaired in chemokine mRNA induction whereas LAT-deficient mast cells showed a more pronounced defect in cytokines. These findings demonstrate that perturbation of small numbers of IgE receptors on mast cells favors certain signals that contribute to a lymphokine response that can mediate allergic inflammation.

Indexed as

AnimalsAntigensCell DegranulationChemokine CCL2ChemokinesCytokinesFemaleHypersensitivityImmunoglobulin EIn Vitro TechniquesLymphokinesMaleMast CellsMiceMice, Inbred C57BLMice, KnockoutAntigensChemokine CCL2ChemokinesCytokinesImmunoglobulin ELymphokinesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesReceptors, IgERNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID12782712
PMCPMC2193904
OpenAlexW2127708908

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.