Evidence map›Paper›PMID 26727515›Full record

ArticlePloS one2016

Immune Alterations in Patients with Anti-Interferon-γ Autoantibodies.

Nuttapol Chruewkamlow, Kodchakorn Mahasongkram, Supansa Pata, Romanee Chaiwarith, Parichart Salee, Khuanchai Supparatpinyo, Watchara Kasinrerk

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Nuttapol ChruewkamlowBiomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, National Sciences and Technology Development Agency at the Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
Kodchakorn MahasongkramBiomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, National Sciences and Technology Development Agency at the Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
Supansa PataBiomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, National Sciences and Technology Development Agency at the Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
Romanee ChaiwarithDepartment of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Parichart SaleeDepartment of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Khuanchai SupparatpinyoDepartment of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Watchara KasinrerkBiomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, National Sciences and Technology Development Agency at the Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
Chiang Mai University · THNational Science and Technology Development Agency · THNational Center for Genetic Engineering and Biotechnology · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoantibodies against interferon-gamma (IFN-γ) can cause immunodeficiency and are associated with various opportunistic infections. In the present study, we investigated other cellular immune parameters for a better understanding of the immunodeficiency condition in the patients. The numbers of WBC, monocytes and NK cells were increased in patients with anti-IFN-γ autoantibodies (AAbs). Upon TCR activation, T cell proliferation and IL-2 receptor of the patients remained intact. Nonetheless, the Th1 cytokine (IFN-γ and TNF-α) production was up-regulated. The production of Th2 (IL-4) and Th17 (IL-17) cytokines was unchanged. We suggest that, in addition to the presence of anti-IFN-γ autoantibodies, alterations in the cellular immune functions may also contribute to this immunodeficiency.

Indexed as

AutoantibodiesCase-Control StudiesCytokinesHumansImmunity, CellularImmunologic Deficiency SyndromesInterferon-gammaT-LymphocytesAutoantibodiesCytokinesInterferon-gamma

Identifiers

PMID26727515
PMCPMC4699769
OpenAlexW2222206255

What OpenQuestion holds

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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.