Evidence map›Paper›PMID 26078984›Full record

ArticleJournal of immunology research2015

HMGB1 Promotes Systemic Lupus Erythematosus by Enhancing Macrophage Inflammatory Response.

Mudan Lu, Shanshan Yu, Wei Xu, Bo Gao, Sidong Xiong

Open access · goldAbstract read
In one paragraph

Article in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Novel Biomarkers for Diagnosis and Monitoring of Immune Thrombocytopenia.International journal of molecular sciences · 2023
    Review
  8. Article
  9. The Role of HMGB1 in Rheumatic Diseases.Frontiers in immunology · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. HMGB1 in Systemic Lupus Erythematosus.Frontiers in immunology · 2020
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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 2 institutions in 1 country.

Mudan LuInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Shanshan YuInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Wei XuJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China.ORCID 0000-0003-2652-8244
Bo GaoInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Sidong XiongInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai 200032, China ; Jiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China.
Shanghai Medical College of Fudan University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/Purpose. HMGB1, which may act as a proinflammatory mediator, has been proposed to contribute to the pathogenesis of multiple chronic inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE); however, the precise mechanism of HMGB1 in the pathogenic process of SLE remains obscure. Method. The expression of HMGB1 was measured by ELISA and western blot. The ELISA was also applied to detect proinflammatory cytokines levels. Furthermore, nephritic pathology was evaluated by H&E staining of renal tissues. Results. In this study, we found that HMGB1 levels were significantly increased and correlated with SLE disease activity in both clinical patients and murine model. Furthermore, gain- and loss-of-function analysis showed that HMGB1 exacerbated the severity of SLE. Of note, the HMGB1 levels were found to be associated with the levels of proinflammatory cytokines such as TNF-α and IL-6 in SLE patients. Further study demonstrated that increased HMGB1 expression deteriorated the severity of SLE via enhancing macrophage inflammatory response. Moreover, we found that receptor of advanced glycation end products played a critical role in HMGB1-mediated macrophage inflammatory response. Conclusion. These findings suggested that HMGB1 might be a risk factor for SLE, and manipulation of HMGB1 signaling might provide a therapeutic strategy for SLE.

Indexed as

AdultAnimalsAntibodies, AntinuclearCase-Control StudiesCell LineCytokinesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleGene ExpressionHMGB1 ProteinHumansInflammation MediatorsLupus Erythematosus, SystemicMacrophagesMaleAntibodies, AntinuclearCytokinesHMGB1 ProteinInflammation MediatorsReceptor for Advanced Glycation End ProductsToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID26078984
PMCPMC4452473
OpenAlexW2102142278

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.