Evidence map›Paper›PMID 24130688›Full record

ArticlePloS one2013

IVIg immune reconstitution treatment alleviates the state of persistent immune activation and suppressed CD4 T cell counts in CVID.

Dominic Paquin-Proulx, Bianca A N Santos, Karina I Carvalho, Myrthes Toledo-Barros, Ana Karolina Barreto de Oliveira, Cristina M Kokron, Jorge Kalil, Markus Moll, Esper G Kallas, Johan K Sandberg

Open access · goldAbstract readControlled Clinical Trial
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Infectious Complications Predict Premature CD8Journal of clinical immunology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Immune deficiency: changing spectrum of pathogens.Clinical and experimental immunology · 2015
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 2 institutions in 2 countries.

Dominic Paquin-ProulxCenter for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Bianca A N Santos
Karina I Carvalho
Myrthes Toledo-Barros
Ana Karolina Barreto de Oliveira
Cristina M Kokron
Jorge Kalil
Markus Moll
Esper G Kallas
Johan K Sandberg
Universidade de São Paulo · BRKarolinska University Hospital · SE

Funding

Innate NKT Cells in HIV InfectionR37AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2007 to 2016
$3.1M
Innate NKT Cells in HIV InfectionR01AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2002 to 2006
$2.1M
CIHRNIAID NIH HHS R01 AI052731NIAID NIH HHS R37 AI052731
6 · The paper itself

Abstract

Common variable immunodeficiency (CVID) is characterized by defective B cell function, impaired antibody production, and increased susceptibility to bacterial infections. Here, we addressed the hypothesis that poor antibody-mediated immune control of infections may result in substantial perturbations in the T cell compartment. Newly diagnosed CVID patients were sampled before, and 6-12 months after, initiation of intravenous immunoglobulin (IVIg) therapy. Treatment-naïve CVID patients displayed suppressed CD4 T cell counts and myeloid dendritic cell (mDC) levels, as well as high levels of immune activation in CD8 T cells, CD4 T cells, and invariant natural killer T (iNKT) cells. Expression of co-stimulatory receptors CD80 and CD83 was elevated in mDCs and correlated with T cell activation. Levels of both FoxP3+ T regulatory (Treg) cells and iNKT cells were low, whereas soluble CD14 (sCD14), indicative of monocyte activation, was elevated. Importantly, immune reconstitution treatment with IVIg partially restored the CD4 T cell and mDC compartments. Treatment furthermore reduced the levels of CD8 T cell activation and mDC activation, whereas levels of Treg cells and iNKT cells remained low. Thus, primary deficiency in humoral immunity with impaired control of microbial infections is associated with significant pathological changes in cell-mediated immunity. Furthermore, therapeutic enhancement of humoral immunity with IVIg infusions alleviates several of these defects, indicating a relationship between poor antibody-mediated immune control of infections and the occurrence of abnormalities in the T cell and mDC compartments. These findings help our understanding of the immunopathogenesis of primary immunodeficiency, as well as acquired immunodeficiency caused by HIV-1 infection.

Indexed as

AdultAgedAntigens, CDB7-1 AntigenCD4-Positive T-LymphocytesCD83 AntigenCD8-Positive T-LymphocytesCommon Variable ImmunodeficiencyFemaleHumansImmunity, HumoralImmunoglobulinsImmunoglobulins, IntravenousLipopolysaccharide ReceptorsMaleMembrane GlycoproteinsAntigens, CDB7-1 AntigenCD83 AntigenImmunoglobulinsImmunoglobulins, IntravenousLipopolysaccharide ReceptorsMembrane Glycoproteins

Identifiers

PMID24130688
PMCPMC3793979
OpenAlexW2040886654

What OpenQuestion holds

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LicenceCC BY
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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.