Evidence map›Paper›PMID 31921101›Full record

ReviewFrontiers in immunology2019

Current Understanding and Recent Developments in Common Variable Immunodeficiency Associated Autoimmunity.

Jessica D Gereige, Paul J Maglione

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.2field-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

42 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
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  14. IgDPathogens (Basel, Switzerland) · 2024
    Article
  15. Immunological Evaluation of Pediatric Patients with Polyautoimmunity.Endocrine, metabolic & immune disorders drug targets · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. [Autoimmunity and Freiburg classification in common variable immunodeficiency].Revista medica del Instituto Mexicano del Seguro Social · 2023
    Observational
  20. 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

2 authors at 2 institutions in 1 country.

Jessica D GereigeDepartment of Pulmonary, Allergy, Sleep & Critical Care Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, United States.
Paul J MaglioneDepartment of Pulmonary, Allergy, Sleep & Critical Care Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, United States.
Boston Medical Center · USBoston University · US

Funding

BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3M
Role of B cell activating factor in non-infectious complications of common variable immunodeficiencyK23AI137183 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MAGLIONE, PAUL JOSEPH · 2018 to 2022
$945k
NHLBI NIH HHS T32 HL007035NIAID NIH HHS K23 AI137183
6 · The paper itself

Abstract

Common variable immunodeficiency (CVID) is the most prevalent symptomatic primary immunodeficiency and comprises a group of disorders with similar antibody deficiency but a myriad of different etiologies, most of which remain undefined. The variable aspect of CVID refers to the approximately half of patients who develop non-infectious complications in addition to heightened susceptibility to infection. The pathogenesis of these complications is poorly understood and somewhat counterintuitive because these patients that are defined by their immune futility simultaneously have elevated propensity for autoimmune disease. There are numerous aspects of immune dysregulation associated with autoimmunity in CVID that have only begun to be studied. These findings include elevations of T helper type 1 and follicular helper T cells and B cells expressing low levels of CD21 as well as reciprocal decreases in regulatory T cells and isotype-switched memory B cells. Recently, advances in genomics have furthered our understanding of the fundamental biology underlying autoimmunity in CVID and led to precision therapeutic approaches. However, these genetic etiologies are also associated with clinical heterogeneity and incomplete penetrance, highlighting the fact that continued research efforts remain necessary to optimize treatment. Additional factors, such as commensal microbial dysbiosis, remain to be better elucidated. Thus, while recent advances in our understanding of CVID-associated autoimmunity have been exciting and substantial, these current scientific advances must now serve as building blocks for the next stages of discovery.

Indexed as

AutoimmunityDisease SusceptibilityAnimalsAutoimmune DiseasesBiomarkersB-LymphocytesCommon Variable ImmunodeficiencyDisease ManagementGenetic Predisposition to DiseaseHumansImmunophenotypingMicrobiotaT-LymphocytesBiomarkersautoimmunitycommon variable immunodeficiencycytopeniageneticsmicrobiomeprecision therapyprimary immunodeficieny

Identifiers

PMID31921101
PMCPMC6914703
OpenAlexW2989913526

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.