Evidence map›Paper›PMID 19479826›Full record

ArticleArthritis and rheumatism2009

Prolactin alters the mechanisms of B cell tolerance induction.

Subhrajit Saha, Juana Gonzalez, Gabriel Rosenfeld, Harold Keiser, Elena Peeva

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. The crucial role of prolactin-lactogenic hormone in Covid-19.Molecular and cellular biochemistry · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Dopaminergic Agents in Rheumatoid Arthritis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  17. Article
  18. Review
  19. Article
  20. Sex bias in autoimmunity.Current opinion in rheumatology · 2019
    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

5 authors at 1 institution in 1 country.

Subhrajit SahaAlbert Einstein College of Medicine, Bronx, New York, USA.
Juana Gonzalez
Gabriel Rosenfeld
Harold Keiser
Elena Peeva
Albert Einstein College of Medicine · US

Funding

Modulation of B Cell Function by ProlactinK08AI057924 · NIAID · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI PEEVA, ELENA · 2004 to 2007
$500k
NIAID NIH HHS AI-057924NIAID NIH HHS K08 AI057924
6 · The paper itself

Abstract

objectiveAutoimmune diseases predominantly affect women, suggesting that female sex hormones may play a role in the pathogenesis of such diseases. We have previously shown that persistent mild-to-moderate elevations in serum prolactin levels induce a break in self tolerance in mice with a BALB/c genetic background. The aim of this study was to evaluate the effects of hyperprolactinemia on the mechanisms of B cell tolerance induction.

methodsEffects of prolactin on splenic B cell subsets were studied in female BALB/c mice. B cell receptor (BCR)-mediated apoptosis and proliferation of transitional B cells were analyzed by flow cytometry. Expression of apoptotic genes was examined by microarrays and real-time polymerase chain reaction analysis. B cells coexpressing kappa/lambda light chains were assessed by flow cytometry and immunohistochemistry. Activation status of transitional type 3 (T3) B cells was evaluated by BCR-induced calcium influx studies.

resultsBCR-mediated apoptosis of the T1 B cell subset, a major checkpoint for negative selection of autoreactive specificities, was decreased in prolactin-treated mice. Microarray studies indicated that this event may be mediated by the prolactin-induced up-regulation of the antiapoptotic gene interferon-gamma receptor type II and down-regulation of the proapoptotic gene Trp63. Prolactin treatment also altered the amount of receptor editing, as indicated by the increased number of transitional B cells coexpressing kappa/lambda light chains. Additionally, hyperprolactinemia modified the level of B cell anergy by increasing the degree of BCR-induced calcium influx in the T3 B cells.

conclusionPersistently elevated serum prolactin levels interfere with B cell tolerance induction by impairing BCR-mediated clonal deletion, deregulating receptor editing, and decreasing the threshold for activation of anergic B cells, thereby promoting autoreactivity.

Indexed as

AnimalsApoptosisB-LymphocytesCell ProliferationDisease Models, AnimalFemaleHyperprolactinemiaImmune ToleranceImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsInterferon gamma ReceptorMiceMice, Inbred BALB CPhosphoproteinsProlactinReceptors, InterferonImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsInterferon gamma ReceptorPhosphoproteinsProlactinReceptors, InterferonTrans-ActivatorsTrp63 protein, mouse

Identifiers

PMID19479826
PMCPMC2733916
OpenAlexW2027364786

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.