Evidence map›Paper›PMID 36097969›Full record

ArticleJournal of clinical laboratory analysis2022

High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B-cell-activating factor.

Shu Liu, Jing-Jing Miao, Xiao Zhou, Qi Sun, Xiao-Ming Mao

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. A Predictive Model for Graves' Disease Recurrence After Antithyroid Drug Therapy: A Retrospective Multicenter Cohort Study.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025
    Observational
  2. Article
  3. 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

5 authors at 1 institution in 1 country.

Shu LiuDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0002-4649-4400
Jing-Jing MiaoDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Xiao ZhouDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Qi SunDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Xiao-Ming MaoDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0001-7485-5245
Nanjing Medical University · CN

Funding

National Natural Science Foundation of China 81570710
6 · The paper itself

Abstract

backgroundElevated thyroid hormone (TH) levels have been suggested to be associated with the pathological progression of Graves' disease (GD). However, direct evidence from clinical studies remains unclear.

methodsPeripheral blood samples were collected from patients with or without the recurrence of Graves' hyperthyroidism (GH) and healthy donors. Thyroid tissue samples were obtained from patients with benign thyroid nodules. To assess the differentiation of autoreactive B cells, the expression of B-cell-activating factor (BAFF) and the proportion of CD11c+/-IgG+/- subsets of B cells stimulated by high levels of triiodothyronine (T3) in vivo and in vitro were examined by ELISA, flow cytometry, western blotting, and qRT-PCR.

resultsSerum BAFF levels in patients with GD were significantly and positively correlated with FT3, FT4, and TRAb levels. Furthermore, the ratio of abnormally differentiated CD11c+ autoreactive B cells positively correlated with BAFF and TRAb. High levels of triiodothyronine (T3) induced BAFF overexpression in thyroid follicular cells and mononuclear cells of the normal thyroid in vitro, thereby promoting the differentiation of CD11c+IgG+ autoreactive secretory B cells (ASCs). However, the precise knockdown of BAFF expression significantly inhibited the abnormal differentiation of ASCs.

conclusionThe pathological progression of GD was prolonged and exacerbated by autoimmune positive feedback modulation caused by high TH levels. BAFF could be considered a potential target for localized thyroid immunosuppressive treatment of Graves' hyperthyroidism recurrence.

Indexed as

Graves DiseaseHyperthyroidismHumansImmunoglobulin GInterleukin-4ThyroxineTriiodothyronineImmunoglobulin GInterleukin-4ThyroxineTriiodothyronineabnormal differentiation of B cellsautoreactive antibody-secreting B cellsCD11cGraves' hyperthyroidismtriiodothyronine

Identifiers

PMID36097969
PMCPMC9550970
OpenAlexW4295514006

What OpenQuestion holds

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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.