Evidence map›Paper›PMID 20543597›Full record

ReviewCurrent opinion in HIV and AIDS2010

Th17 cells, Job's syndrome and HIV: opportunities for bacterial and fungal infections.

Joshua D Milner, Netanya G Sandler, Daniel C Douek

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in HIV and AIDS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Inflammation and immune system interactions in atherosclerosis.Cellular and molecular life sciences : CMLS · 2013
    Review
  17. Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Joshua D MilnerAllergic Inflammation Unit, Laboratory of Allergic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Netanya G Sandler
Daniel C Douek
National Institute of Allergy and Infectious Diseases · US

Funding

T Cell Immune Responses To HIV And Other PathogensZIAAI005033 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DOUEK, DANIEL CESAR · 2009 to 2025
$11.4M
The HIV ReservoirZIAAI005034 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DOUEK, DANIEL CESAR · 2009 to 2025
$7.5M
Pathogenesis and Treatment of Atopic DermatitisZIAAI001098 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MILNER, JOSHUA · 2009 to 2019
$6.5M
InflammationZIAAI005031 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DOUEK, DANIEL CESAR · 2009 to 2024
$5.9M
Intramural NIH HHS ZIA AI005033
6 · The paper itself

Abstract

purpose of reviewPatients with hyper IgE syndrome (HIES) share with HIV patients a predisposition to infections, including candidiasis in autosomal dominant HIES (AD-HIES) and molluscum contagiosum and other viral infections in other disorders of elevated IgE with infectious predilections. This review highlights the underlying pathogenesis of these diseases and their relevance to HIV infection. RECENT

findingsPatients with mutations in STAT3, who lack Th17 cells, develop AD-HIES, whereas other disorders of elevated IgE may be caused by mutations in Tyk2 or DOCK8, the latter of which is associated with decreased expansion of CD8 more so than CD4 T cells. Recent studies on patients with recurrent mucocutaneous candidiasis have led to the discovery of mutations in CARD9 and DECTIN-1, genes key to the production of the Th17-driving cytokines IL-1beta, IL-6, and IL-23. Studies of the peripheral blood of HIV-positive patients have shown a decreased Th17:Th1 ratio, and Th17 cells were preferentially depleted from the gastrointestinal tract within weeks of simian immunodeficiency virus infection in rhesus macaques. SUMMARY: The consequences of inadequate Th17 production in primary immunodeficiency syndromes illustrate the role of Th17 cells in controlling pathogens to which HIV-positive individuals are susceptible. Further understanding of the pathogenesis of opportunistic disease in HIV infection will probably require exploring the role of Th17 cells.

Indexed as

CARD Signaling Adaptor ProteinsDectin-1Guanine Nucleotide Exchange FactorsHIV InfectionsHumansImmunoglobulin EInterleukin-1betaInterleukin-23Interleukin-6Job SyndromeLectins, C-TypeMembrane ProteinsNerve Tissue ProteinsSTAT3 Transcription FactorT-Lymphocytes, Helper-InducerTYK2 KinaseCARD9 protein, humanCARD Signaling Adaptor ProteinsDectin-1DOCK8 protein, humanGuanine Nucleotide Exchange FactorsImmunoglobulin EInterleukin-1betaInterleukin-23Interleukin-6Lectins, C-TypeMembrane ProteinsNerve Tissue ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTYK2 KinaseTYK2 protein, human

Identifiers

PMID20543597
PMCPMC4485419
OpenAlexW2052659821

What OpenQuestion holds

Textmetadata
LicenceTDM
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.