Evidence map›Paper›PMID 28491063›Full record

ArticleFrontiers in immunology2017

ISA-2011B, a Phosphatidylinositol 4-Phosphate 5-Kinase α Inhibitor, Impairs CD28-Dependent Costimulatory and Pro-inflammatory Signals in Human T Lymphocytes.

Martina Kunkl, Nicla Porciello, Marta Mastrogiovanni, Cristina Capuano, Federica Lucantoni, Chiara Moretti, Jenny L Persson, Ricciarda Galandrini, Raffaella Buzzetti, Loretta Tuosto

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Allergen-induced activation of epithelial P2YThe Journal of allergy and clinical immunology · 2025
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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 3 institutions in 2 countries.

Martina KunklDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Nicla PorcielloDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Marta MastrogiovanniDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Cristina CapuanoDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Federica LucantoniDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Chiara MorettiDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Jenny L PerssonDivision of Experimental Cancer Research, Department of Laboratory Medicine, Clinical Research Center, Lund University, Malmö, Sweden.
Ricciarda GalandriniDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Raffaella BuzzettiDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
Loretta TuostoDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.
Sapienza University of Rome · ITIstituto Pasteur · ITLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphatidylinositol 4,5-biphosphate (PIP2) is a membrane phospholipid that controls the activity of several proteins regulating cytoskeleton reorganization, cytokine gene expression, T cell survival, proliferation, and differentiation. Phosphatidylinositol 4-phosphate 5-kinases (PIP5Ks) are the main enzymes involved in PIP2 biosynthesis by phosphorylating phosphatidylinositol 4-monophosphate (PI4P) at the D5 position of the inositol ring. In human T lymphocytes, we recently found that CD28 costimulatory molecule is pivotal for PIP2 turnover by recruiting and activating PIP5Kα. We also found that PIP5Kα is the main regulator of both CD28 costimulatory signals integrating those delivered by TCR as well as CD28 autonomous signals regulating the expression of pro-inflammatory genes. Given emerging studies linking alterations of PIP2 metabolism to immune-based diseases, PIP5Kα may represent a promising target to modulate immunity and inflammation. Herewith, we characterized a recently discovered inhibitor of PIP5Kα, ISA-2011B, for its inhibitory effects on T lymphocyte functions. We found that the inhibition of PIP5Kα lipid-kinase activity by ISA-2011B significantly impaired CD28 costimulatory signals necessary for TCR-mediated Ca

Indexed as

CD28 co-stimulationPIP5Kpro-inflammatory cytokinesT1DT lymphocytes

Identifiers

PMID28491063
PMCPMC5405084
OpenAlexW2607567181

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.