Evidence map›Paper›PMID 30565247›Full record

ReviewImmunological reviews2019

Common variable immune deficiency: Dissection of the variable.

Charlotte Cunningham-Rundles

Abstract readReview
In one paragraph

Review in Immunological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Coexistent alterations of BAFF and B-cell phenotypes in complicated CVID course.The Journal of allergy and clinical immunology · 2026
    Article
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  12. Cellular and molecular basis of proximal small intestine disorders.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  13. Exploring gastric cancer genetics: A turning point in common variable immunodeficiency.The journal of allergy and clinical immunology. Global · 2024
    Article
  14. Article
  15. Review
  16. Article
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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

1 author.

Charlotte Cunningham-RundlesDivision of Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, New York.ORCID 0000-0003-0725-0320

Funding

Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2004 to 2021
$29.8M
Resources to Assist Investigations in Primary Immunodeficiency Diseases (U24)U24AI086037 · NIAID · IMMUNE DEFICIENCY FOUNDATION · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2010 to 2019
$6.5M
TARGETING PRIMARY IMMUNODEFICIENCY AMONG MINORITIESR18AI048693 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2000 to 2016
$6.2M
NIAID NIH HHS P01 AI061093NIAID NIH HHS R18 AI048693NIAID NIH HHS U24 AI086037
6 · The paper itself

Abstract

Starting about 60 years ago, a number of reports appeared that outlined the severe clinical course of a few adult subjects with profound hypogammaglobinemia. Puzzled by the lack of family history and adult onset of symptoms in most, the name "acquired" hypogammaglobinemia was given, but later altered to the current name common variable immune deficiency. Pathology reports remarked on the loss of lymph node architecture and paucity of plasma cells in lymphoid tissues in these subjects. While characterized by reduced serum IgG and IgA and often IgM, and thus classified among the B-cell defects, an increasing number of cellular defects in these patients have been recognized over time. In the early years, severe respiratory tract infections commonly led to a shortened life span, but the wide spread availability of immune globulin concentrates for the last 25 years has improved survival. However, chronic non-infectious inflammatory and autoimmune conditions have now emerged as challenging clinical problems; these require further immunologic understanding and additional therapeutic measures. Recent study of this phenotypic syndrome have provided an increasingly fertile ground for the identification of autosomal recessive and now more commonly, autosomal dominant gene defects which lead to the loss of B-cell development in this syndrome.

Indexed as

AgammaglobulinemiaAnimalsAutoimmunityB-LymphocytesCell DifferentiationCommon Variable ImmunodeficiencyHumansImmunoglobulins, IntravenousPhenotypeRespiratory Tract InfectionsImmunoglobulins, IntravenousantibodyautoimmunityB-cell developmentcommon variable immune deficiencyenteropathygenetic defectsgeneticsimmune dysregulationimmune globulinnoninfectious complicationsplasma cells

Identifiers

PMID30565247
PMCPMC6435035

What OpenQuestion holds

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Registered trials

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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.