Evidence map›Paper›PMID 38067176›Full record

ReviewCells2023

Th17 Cells, Glucocorticoid Resistance, and Depression.

Julia N Khantakova, Anastasia Mutovina, Kseniya A Ayriyants, Natalia P Bondar

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Epigenetic Signatures of Social Defeat Stress Varying Duration.International journal of molecular sciences · 2025
    Article
  8. Article
  9. Article
  10. Febrile temperature-regulated TRPV1 in CD4Journal of neuroinflammation · 2025
    Article
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  12. 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

4 authors at 2 institutions in 1 country.

Julia N KhantakovaInstitute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences (SB RAS), Prospekt Lavrentyeva 10, Novosibirsk 630090, Russia.ORCID 0000-0001-9281-9002
Anastasia MutovinaDepartment of Natural Sciences, Novosibirsk State University, Pirogova Street 2, Novosibirsk 630090, Russia.ORCID 0009-0001-3908-8332
Kseniya A AyriyantsInstitute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences (SB RAS), Prospekt Lavrentyeva 10, Novosibirsk 630090, Russia.ORCID 0000-0002-9722-3037
Natalia P BondarInstitute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences (SB RAS), Prospekt Lavrentyeva 10, Novosibirsk 630090, Russia.ORCID 0000-0002-5602-5149
Institute of Cytology and Genetics · RUNovosibirsk State University · RU

Funding

Russian Science Foundation 21-15-00142
6 · The paper itself

Abstract

Depression is a severe mental disorder that disrupts mood and social behavior and is one of the most common neuropsychological symptoms of other somatic diseases. During the study of the disease, a number of theories were put forward (monoamine, inflammatory, vascular theories, etc.), but none of those theories fully explain the pathogenesis of the disease. Steroid resistance is a characteristic feature of depression and can affect not only brain cells but also immune cells. T-helper cells 17 type (Th17) are known for their resistance to the inhibitory effects of glucocorticoids. Unlike the inhibitory effect on other subpopulations of T-helper cells, glucocorticoids can enhance the differentiation of Th17 lymphocytes, their migration to the inflammation, and the production of IL-17A, IL-21, and IL-23 in GC-resistant disease. According to the latest data, in depression, especially the treatment-resistant type, the number of Th17 cells in the blood and the production of IL-17A is increased, which correlates with the severity of the disease. However, there is still a significant gap in knowledge regarding the exact mechanisms by which Th17 cells can influence neuroinflammation in depression. In this review, we discuss the mutual effect of glucocorticoid resistance and Th17 lymphocytes on the pathogenesis of depression.

Indexed as

Interleukin-17Th17 CellsDepressionGlucocorticoidsHumansMetabolism, Inborn ErrorsReceptors, GlucocorticoidGlucocorticoidsInterleukin-17Receptors, Glucocorticoiddepressionglucocorticoid resistancegut–brain axisinterleukin-17neuroinflammationT-helper 17 lymphocites

Identifiers

PMID38067176
PMCPMC10706111
OpenAlexW4389205997

What OpenQuestion holds

Textmetadata
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.