Evidence map›Paper›PMID 24600593›Full record

ReviewAdvanced biomedical research2014

Genetic defects and the role of helper T-cells in the pathogenesis of common variable immunodeficiency.

Reza Yazdani, Mazdak Ganjalikhani Hakemi, Roya Sherkat, Vida Homayouni, Rahim Farahani

Open access · goldAbstract readReview
In one paragraph

Review in Advanced biomedical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.3field-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

11 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  5. Central-European journal of immunology · 2018
    Article
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  7. Article
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  11. Evaluation of the T helper 17 cell specific genes and the innate lymphoid cells counts in the peripheral blood of patients with the common variable immunodeficiency.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2014
    Article
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

5 authors at 2 institutions in 1 country.

Reza YazdaniDepartment of Immunology, Faculty of Medicine, Isfahan, Iran.
Mazdak Ganjalikhani HakemiCellular and Molecular Immunology Research Center, Isfahan, Iran ; Department of Immunology, Faculty of Medicine, Isfahan, Iran.
Roya SherkatAcquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Vida HomayouniDepartment of Immunology, Faculty of Medicine, Isfahan, Iran.
Rahim FarahaniDepartment of Immunology, Faculty of Medicine, Isfahan, Iran.
University of Isfahan · IRIsfahan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Common variable immunodeficfiiency (CVID) is a primary immunodeficiency syndrome representing a heterogeneous set of disorders resulting mostly in antibody deficiency and recurrent infections. However, inflammatory and autoimmune disorders and some kinds of malignancies are frequently reported as a part of the syndrome. Although it is one of the most widespread primary immunodeficiency, only recently some genetic defects in CVID have been identified. Mutations have been detected in inducible T-cell costimulator (ICOS), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), B-cell activating factor-receptor (BAFF-R), B-cell receptor complex (CD19, CD21 and CD81) and CD20. On the other hand, recent studies have shown a decrease in T-helper-17 cells frequency and their characteristic cytokines in CVID patients and this emphasis on the vital role of the T-cells in immunopathogenesis of the CVID. Furthermore, in the context of autoimmune diseases accompanying CVID, interleukin 9 has recently attracted a plenty of considerations. However, the list of defects is expanding as exact immunologic pathways and genetic disorders in CVID are not yet defined. In this review, we have a special focus on the immunopathogenesis of CVID, recent advances in understanding the underlying etiology and genetics for patients.

Indexed as

B-cell activating factor receptorcommon variable immunodeficiencyinducible T-cell co-stimulatorinterleukin 9T-helper-17transmembrane activator and calcium modulator and cyclophilin ligand interactor

Identifiers

PMID24600593
PMCPMC3929019
OpenAlexW2089355077

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.