Evidence map›Paper›PMID 19538479›Full record

ArticleJournal of cellular and molecular medicine2010

Methylglyoxal modulates immune responses: relevance to diabetes.

Claire L Price, Hafid O S Al Hassi, Nicholas R English, Alexandra I F Blakemore, Andrew J Stagg, Stella C Knight

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05135676 (Time in Glucose Hospital Target), which is not on this map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
1.6field-weighted citation impact, top 20% 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.

NCT05135676 nacompletednot on this mapstarted 2022, after this paper: background citation

Time in Glucose Hospital Target (TIGHT) - A Randomized Clinical Trial to Evaluate the Use of CGM to Achieve a Mean Glucose Target of 90 to 130 mg/dL Without Hypoglycemia in Hospitalized Adults With Type 2 Diabetes

TypeinterventionalSponsorJaeb Center for Health ResearchRan2022 to 2024Enrolled169ConditionsDiabetes Mellitus, Type 2ArmsBlinded CGM, real-time CGM
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Article
  5. Autoimmune Diseases and Mycobacterial Infection.Diseases (Basel, Switzerland) · 2026
    Review
  6. Review
  7. Article
  8. Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  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

6 authors at 2 institutions in 1 country.

Claire L PriceAntigen Presentation Research Group, Imperial College London, Northwick Park and St. Marks Campus, Harrow, Middlesex, UK.
Hafid O S Al Hassi
Nicholas R English
Alexandra I F Blakemore
Andrew J Stagg
Stella C Knight
St Mark's Hospital · GBHammersmith Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased methylglyoxal (MG) concentrations and formation of advanced glycation end-products (AGEs) are major pathways of glycaemic damage in diabetes, leading to vascular and neuronal complications. Diabetes patients also suffer increased susceptibility to many common infections, the underlying causes of which remain elusive. We hypothesized that immune glycation damage may account for this increased susceptibility. We previously showed that the reaction mixture (RM) for MG glycation of peptide blocks up regulation of CD83 in myeloid cells and inhibits primary stimulation of T cells. Here, we continue to investigate immune glycation damage, assessing surface and intracellular cytokine protein expression by flow cytometry, T-cell proliferation using a carboxyfluorescein succinimidyl ester assay, and mRNA levels by RT-PCR. We show that the immunomodulatory component of this RM was MG itself, with MG alone causing equivalent block of CD83 and loss of primary stimulation. Block of CD83 expression could be reversed by MG scavenger N-acetyl cysteine. Further, MG within RM inhibited stimulated production of interleukin (IL)-10 protein from myeloid cells plus interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha from T cells. Loss of IL-10 and IFN-gamma was confirmed by RT-PCR analysis of mRNA, while TNF-alpha message was raised. Loss of TNF-alpha protein was also shown by ELISA of culture supernatants. In addition, MG reduced major histocompatibility complex (MHC) class I expression on the surface of myeloid cells and increased their propensity to apoptose. We conclude that MG is a potent suppressor of myeloid and T-cell immune function and may be a major player in diabetes-associated susceptibility to infection.

Indexed as

Antigens, CDApoptosisCD83 AntigenCell ProliferationCytokinesDiabetes MellitusGene Expression RegulationHistocompatibility Antigens Class IHumansImmunoglobulinsImmunomodulationMembrane GlycoproteinsMyeloid CellsPyruvaldehydeRNA, MessengerT-LymphocytesAntigens, CDCD83 AntigenCytokinesHistocompatibility Antigens Class IImmunoglobulinsMembrane GlycoproteinsPyruvaldehydeRNA, Messenger

Identifiers

PMID19538479
PMCPMC3829040
OpenAlexW2039942462

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.