ReviewSeminars in immunopathology2016
Regulation of allergic inflammation by the ectoenzyme E-NPP3 (CD203c) on basophils and mast cells.
Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- CD25 expression marks an activated mast cell population in human nasal polyposis.The Journal of allergy and clinical immunology · 2026Article
- [Allergens induce activation of blood CCR3Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Article
- A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Degranulation of human mast cells: modulation by P2 receptors' agonists.Frontiers in immunology · 2023Review
- The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023Article
- Perinatal and Early-Life Nutrition, Epigenetics, and Allergy.Nutrients · 2021Review
- Impaired Expression of Ectonucleotidases in Ectopic and Eutopic Endometrial Tissue Is in Favor of ATP Accumulation in the Tissue Microenvironment in Endometriosis.International journal of molecular sciences · 2019Article
- Adventitial Cell Atlas of wt (Wild Type) and ApoE (Apolipoprotein E)-Deficient Mice Defined by Single-Cell RNA Sequencing.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- In vitro and in vivo efficacy of an anti-CD203c conjugated antibody (AGS-16C3F) in mouse models of advanced systemic mastocytosis.Blood advances · 2019Article
- Article
- Basophils and mast cells in immunity and inflammation.Seminars in immunopathology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine 5'-triphosphate (ATP) is released from dying or damaged cells, as well as from activated cells. Once secreted, extracellular ATP induces several immune responses via P2X and P2Y receptors. Basophils and mast cells release ATP upon FcεRI-crosslinking, and ATP activates basophils and mast cells in an autocrine manner. Nucleotide-converting ectoenzymes, such as E-NTPD1, E-NTPD7, and E-NPP3, inhibit ATP-dependent immune responses by hydrolyzing ATP, thereby contributing to immune response regulation. E-NPP3 is a well-known activation marker for human basophils. E-NPP3's physiologic function has recently been disclosed in mice. E-NPP3 is rapidly induced on basophils and mast cells after FcεRI-crosslinking and hydrolyzes extracellular ATP on cell surfaces to prevent ATP-dependent excess activation of basophils and mast cells. In the absence of E-NPP3, basophils and mast cells are overactivated and mice suffer from severe chronic allergic inflammation. Thus, the ATP-hydrolyzing ectoenzymes E-NPP3 has a nonnegligible role in the regulation of basophil- and mast cell-mediated allergic responses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.