Evidence map›Paper›PMID 30465180›Full record

ReviewJournal of clinical immunology2019

Autoimmunity and Inflammation in CVID: a Possible Crosstalk between Immune Activation, Gut Microbiota, and Epigenetic Modifications.

Silje F Jørgensen, Børre Fevang, Pål Aukrust

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Article
  8. Review
  9. Article
  10. Common variable immunodeficiency: autoimmune cytopenias and advances in molecular diagnosis.Hematology. American Society of Hematology. Education Program · 2024
    Review
  11. Article
  12. Immunogenetic Landscape in Pediatric Common Variable Immunodeficiency.International journal of molecular sciences · 2024
    Review
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  16. Review
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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

3 authors at 1 institution in 1 country.

Silje F JørgensenResearch Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital, Rikshospitalet, Nydalen, P.O. Box 4950, 0424, Oslo, Norway. s.f.jorgensen@medisin.uio.no.ORCID 0000-0002-0968-7051
Børre FevangResearch Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital, Rikshospitalet, Nydalen, P.O. Box 4950, 0424, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital, Rikshospitalet, Nydalen, P.O. Box 4950, 0424, Oslo, Norway.
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Common variable immunodeficiency (CVID) is the most common symptomatic primary immunodeficiency among adults and is characterized by a B cell dysfunction and increased risk of respiratory tract infections with encapsulated bacteria. However, a large proportion of patients also has inflammatory and autoimmune complications. It may seem like a paradox that immunodeficiency and inflammation/autoimmunity coexist within the same individuals. In this commentary, we propose that CVID immunopathogenesis involves an interplay of genes, environmental factors, and dysregulation of immune cells, where gut microbiota and gastrointestinal inflammation can both be important contributors or endpoints to the systemic immune activation seen in CVID, and where epigenetic mechanism may be the undiscovered link between these contributors. In our opinion, these pathways could represent novel targets for therapy in CVID directed against autoimmune and inflammatory manifestations that represent the most severe complications in these patients. Considering the heterogeneous nature of CVID, these mechanisms may not be present in all patients, and different complications may be triggered by different risk factors. CVID is really a variable disease and in the future there is clearly a need for a more personalized medicine based on both genotypic and phenotypic findings.

Indexed as

AnimalsAutoimmunityCinnamatesCommon Variable ImmunodeficiencyCross ReactionsEpigenesis, GeneticGastrointestinal MicrobiomeGenotypeHumansImidazolesInflammationPhenotypeanimacroxamCinnamatesImidazolesautoimmunityCommon variable immunodeficiencyepigeneticgut microbiotainflammationmucosal immunologyPrimary immunodeficinecy

Identifiers

PMID30465180
OpenAlexW2900534518

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.