Evidence map›Paper›PMID 16630927›Full record

ReviewThe Journal of allergy and clinical immunology2006

Molecular basis of common variable immunodeficiency.

Emanuela Castigli, Raif S Geha

Abstract readReview
PubMed Publisher
In one paragraph

Review in The Journal of allergy and clinical immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Antibody deficiency associated with an inherited autosomal dominant mutation in TWEAK.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  3. Immune abnormalities in IgA nephropathy.Clinical kidney journal · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Development, manufacturing and characterization of a highly purified, liquid immunoglobulin g preparation from human plasma.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2014
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Clinical consequences of defects in B-cell development.The Journal of allergy and clinical immunology · 2010
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Emanuela CastigliDivision of Immunology, Children's Hospital, Boston, Massachusetts 02115, USA. emanuela.castigli@childrens.harvard.edu
Raif S Geha
Boston Children's Hospital · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Common variable immunodeficiency (CVID) is the most prevalent human primary immunodeficiency requiring medical attention. Until recently, the only known genetic defect specific to CVID was the inducible costimulatory receptor (ICOS) deficiency, which accounts for less than 1% of the patients. Recently, mutations in the TNF receptor family member transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), which mediates isotype switching in B cells, were found to be present in 10% to 20% of patients with CVID. Mutations in TACI were also found in relatives of patients with CVID who had IgA deficiency (IgAD), as well as in a patient with isolated IgAD. In the majority of patients described to date, only one TACI allele is mutated, showing an autosomal dominant transmission of the disease. B cells from individuals with TACI mutations did not produce IgG and IgA in response to the TACI ligand a proliferation-inducing ligand (APRIL), probably reflecting impaired isotype switching. These results suggest that TACI mutations can lead to CVID and IgAD.

Indexed as

AnimalsB-Cell Activating FactorB-Cell Activation Factor ReceptorB-LymphocytesCell DifferentiationCommon Variable ImmunodeficiencyHumansIgA DeficiencyImmunoglobulin Class SwitchingMembrane ProteinsMiceMutationPlasma CellsReceptors, Tumor Necrosis FactorTransmembrane Activator and CAML Interactor ProteinTumor Necrosis Factor-alphaB-Cell Activating FactorB-Cell Activation Factor ReceptorMembrane ProteinsReceptors, Tumor Necrosis FactorTNFRSF13B protein, humanTNFRSF13C protein, humanTNFSF13B protein, humanTnfsf13b protein, mouseTNFSF13 protein, humanTransmembrane Activator and CAML Interactor ProteinTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID16630927
OpenAlexW2106191188

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.