Evidence map›Paper›PMID 26453379›Full record

ArticleImmunity2015

Wiskott-Aldrich Syndrome Interacting Protein Deficiency Uncovers the Role of the Co-receptor CD19 as a Generic Hub for PI3 Kinase Signaling in B Cells.

Selina Jessica Keppler, Francesca Gasparrini, Marianne Burbage, Shweta Aggarwal, Bruno Frederico, Raif S Geha, Michael Way, Andreas Bruckbauer, Facundo D Batista

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2015. 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
5.1field-weighted citation impact, top 4% 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, 70 citations in OpenAlex.

  1. Article
  2. TACI regulates marginal zone B cell development.The Journal of experimental medicine · 2026
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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

9 authors at 3 institutions in 2 countries.

Selina Jessica KepplerLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Francesca GasparriniLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Marianne BurbageLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Shweta AggarwalLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Bruno FredericoLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Raif S GehaDivision of Immunology, Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Michael WayCell Motility Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Andreas BruckbauerLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
Facundo D BatistaLymphocyte Interaction Laboratory, The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK. Electronic address: facundo.batista@crick.ac.uk.
The Francis Crick Institute · GBThe Honourable Society of Lincoln's Inn · GBBoston Children's Hospital · US

Funding

Cancer Research UK 15691
6 · The paper itself

Abstract

Humans with Wiskott-Aldrich syndrome display a progressive immunological disorder associated with compromised Wiskott-Aldrich Syndrome Interacting Protein (WIP) function. Mice deficient in WIP recapitulate such an immunodeficiency that has been attributed to T cell dysfunction; however, any contribution of B cells is as yet undefined. Here we have shown that WIP deficiency resulted in defects in B cell homing, chemotaxis, survival, and differentiation, ultimately leading to diminished germinal center formation and antibody production. Furthermore, in the absence of WIP, several receptors, namely the BCR, BAFFR, CXCR4, CXCR5, CD40, and TLR4, were impaired in promoting CD19 co-receptor activation and subsequent PI3 kinase (PI3K) signaling. The underlying mechanism was due to a distortion in the actin and tetraspanin networks that lead to altered CD19 cell surface dynamics. In conclusion, our findings suggest that, by regulating the cortical actin cytoskeleton, WIP influences the function of CD19 as a general hub for PI3K signaling.

Indexed as

Actin CytoskeletonActinsAnimalsAntibody FormationAntigens, CD19B-LymphocytesCarrier ProteinsCells, CulturedChemokinesChemotaxisCytoskeletal ProteinsGerminal CenterHaptensHemocyaninsLymphocyte ActivationLymphopoiesis4-hydroxy-3-nitrophenylacetyl-keyhole limpet hemocyaninActinsAntigens, CD19Carrier ProteinsChemokinesCytoskeletal ProteinsHaptensHemocyaninsMembrane ProteinsPhosphatidylinositol 3-KinasesReceptors, Antigen, B-CellReceptors, ChemokineTetraspaninsWaspip protein, mouse

Identifiers

PMID26453379
PMCPMC4622935
OpenAlexW1842275027

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.