Evidence map›Paper›PMID 23607751›Full record

ArticleClinical and experimental immunology2013

Mesenchymal stem cells (MSCs) from scleroderma patients (SSc) preserve their immunomodulatory properties although senescent and normally induce T regulatory cells (Tregs) with a functional phenotype: implications for cellular-based therapy.

P Cipriani, P Di Benedetto, V Liakouli, B Del Papa, M Di Padova, M Di Ianni, A Marrelli, E Alesse, R Giacomelli

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Stem cell therapy in systemic sclerosis.Clinical rheumatology · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

P CiprianiDepartment of Biothecnological and Applied Clinical Science, Rheumatology Unit, School of Medicine, University of L'Aquila, L'Aquila,. Italy paola.cipriani@cc.univaq.it
P Di Benedetto
V Liakouli
B Del Papa
M Di Padova
M Di Ianni
A Marrelli
E Alesse
R Giacomelli
University of L'Aquila · ITUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a chronic disease, with early activation of the immune system. The aim of our work was to address how SSc-mesenchymal stem cells (MSCs), although senescent, might preserve specific immunomodulatory abilities during SSc. MSCs were obtained from 10 SSc patients and 10 healthy controls (HC). Senescence was evaluated by assessing cell cycle, β-galactosidase (β-Gal) activity, p21 and p53 expression; doxorubicin was used as acute senescence stimulus to evaluate their ability to react in stressed conditions. Immunomodulatory abilities were studied co-culturing MSCs with peripheral blood mononuclear cells (PBMCs) and CD4(+) cells, in order to establish both their ability to block proliferation in mixed lymphocyte reaction and in regulatory T cells (Tregs) induction. SSc-MSC showed an increase of senescence biomarkers. Eighty per cent of MSCs were in G0-G1 phase, without significant differences between SSc and HC. SSc-MSCs showed an increased positive β-Gal staining and higher p21 transcript level compared to HC cells. After doxorubicin, β-Gal staining increased significantly in SSc-MSCs. On the contrary, doxorubicin abolished p21 activation and elicited p53 induction both in SSc- and HC-MSCs. Interleukin (IL)-6 and transforming growth factor (TGF)-β-related transcripts and their protein levels were significantly higher in SSc-MSCs. The latter maintained their immunosuppressive effect on lymphocyte proliferation and induced a functionally regulatory phenotype on T cells, increasing surface expression of CD69 and restoring the regulatory function which is impaired in SSc. Increased activation of the IL-6 pathway observed in our cells might represent an adaptive mechanism to senescence, but preserving some specific cellular functions, including immunosuppression.

Indexed as

Antigens, CDAntigens, Differentiation, T-Lymphocytebeta-GalactosidaseCD69 AntigensCell- and Tissue-Based TherapyCell ProliferationCells, CulturedCellular SenescenceCoculture TechniquesCyclin-Dependent Kinase Inhibitor p21DoxorubicinHumansImmunomodulationInterleukin-6Lectins, C-TypeMesenchymal Stem CellsAntigens, CDAntigens, Differentiation, T-Lymphocytebeta-GalactosidaseCD69 AntigensCyclin-Dependent Kinase Inhibitor p21DoxorubicinInterleukin-6Lectins, C-TypeTransforming Growth Factor betaTumor Suppressor Protein p53immunomodulatory abilitiesmesenchymal stem cellssenescencesystemic sclerosis

Identifiers

PMID23607751
PMCPMC3722920
OpenAlexW1577600434

What OpenQuestion holds

Textmetadata
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.