Evidence map›Paper›PMID 37401759›Full record

ArticleeLife2023

The role of B cells in immune cell activation in polycystic ovary syndrome.

Angelo Ascani, Sara Torstensson, Sanjiv Risal, Haojiang Lu, Gustaw Eriksson, Congru Li, Sabrina Teschl, Joana Menezes, Katalin Sandor, Claes Ohlsson and 5 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  13. Androgens Modulate the Immune Profile in a Mouse Model of Polycystic Ovary Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  14. Review
  15. Polycystic ovary syndrome.Nature reviews. Disease primers · 2024
    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

15 authors at 3 institutions in 2 countries.

Angelo Ascani *Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Sara Torstensson *Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0003-4389-2662
Sanjiv RisalDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Haojiang LuDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Gustaw ErikssonDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0003-0120-9028
Congru LiDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Sabrina TeschlDepartment of Internal Medicine, Medical University of Graz, Graz, Austria.
Joana MenezesDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Katalin SandorDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0003-3228-6907
Claes OhlssonCentre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Camilla I SvenssonDepartment of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Mikael C I KarlssonDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Martin Helmut StradnerDepartment of Internal Medicine, Medical University of Graz, Graz, Austria.
Barbara Obermayer-Pietsch *Department of Internal Medicine, Medical University of Graz, Graz, Austria.ORCID 0000-0003-3543-1807
Elisabet Stener-Victorin *Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0002-3424-1502
Karolinska Institutet · SEMedical University of Graz · ATSahlgrenska University Hospital · SE

Funding

Austrian Science Fund FWF W1241European Research Council 866075
6 · The paper itself

Abstract

Variations in B cell numbers are associated with polycystic ovary syndrome (PCOS) through unknown mechanisms. Here, we demonstrate that B cells are not central mediators of PCOS pathology and that their frequencies are altered as a direct effect of androgen receptor activation. Hyperandrogenic women with PCOS have increased frequencies of age-associated double-negative B memory cells and increased levels of circulating immunoglobulin M (IgM). However, the transfer of serum IgG from women into wild-type female mice induces only an increase in body weight. Furthermore, RAG1 knockout mice, which lack mature T- and B cells, fail to develop any PCOS-like phenotype. In wild-type mice, co-treatment with flutamide, an androgen receptor antagonist, prevents not only the development of a PCOS-like phenotype but also alterations of B cell frequencies induced by dihydrotestosterone (DHT). Finally, B cell-deficient mice, when exposed to DHT, are not protected from developing a PCOS-like phenotype. These results urge further studies on B cell functions and their effects on autoimmune comorbidities highly prevalent among women with PCOS.

Indexed as

Polycystic Ovary SyndromeAndrogensAnimalsBody WeightFemaleHumansMicePhenotypeAndrogensandrogensB cellshumanimmuneimmunologyinflammationmousepolycystic ovary syndrome

Identifiers

PMID37401759
PMCPMC10359092
OpenAlexW4383058056

What Socratic 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 Socratic graph.