Evidence map›Paper›PMID 30053831›Full record

ArticleArthritis research & therapy2018

Effects of CTLA4-Ig treatment on circulating fibrocytes and skin fibroblasts from the same systemic sclerosis patients: an in vitro assay.

Maurizio Cutolo, Stefano Soldano, Paola Montagna, Amelia Chiara Trombetta, Paola Contini, Barbara Ruaro, Alberto Sulli, Stefano Scabini, Emanuela Stratta, Sabrina Paolino and 3 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
  6. Upcoming treatments for morphea.Immunity, inflammation and disease · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

13 authors at 3 institutions in 2 countries.

Maurizio CutoloResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy. mcutolo@unige.it.
Stefano SoldanoResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Paola MontagnaResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Amelia Chiara TrombettaResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Paola ContiniDivision of Clinical Immunology, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Barbara RuaroResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Alberto SulliResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Stefano ScabiniOncologic Surgery, Department of Surgery, IRCCS San Martino Polyclinic, Genoa, Italy.
Emanuela StrattaOncologic Surgery, Department of Surgery, IRCCS San Martino Polyclinic, Genoa, Italy.
Sabrina PaolinoResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Carmen PizzorniResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Vanessa SmithDepartment of Rheumatology, Ghent University Hospital, Ghent University, Ghent, Belgium.
Renata BrizzolaraResearch Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genoa, IRCCS San Martino Polyclinic Hospital, Viale Benedetto XV, 616132, Genoa, Italy.
Ospedale Policlinico San Martino · ITUniversity of Genoa · ITGhent University Hospital · BE

Funding

Bristol-Myers Squibb contract number: 30942839
6 · The paper itself

Abstract

backgroundSystemic sclerosis (SSc) is characterized by vasculopathy and progressive fibrosis. CTLA4-Ig (abatacept) is able to interact with the cell surface costimulatory molecule CD86 and downregulate the target cell. The aim of this study was to evaluate the in-vitro effects of CTLA4-Ig treatment on circulating fibrocytes and skin fibroblasts isolated from the same SSc patient.

methodsCirculating fibrocytes and skin fibroblasts were obtained from eight SSc patients with "limited" cutaneous involvement and from four healthy subjects (HSs). Samples were analyzed by fluorescence-activated cell sorter analysis (FACS) at baseline (T0) and after 8 days of culture (T8) for CD45, collagen type I (COL I), CXCR4, CD14, CD86, and HLA-DRII expression. Circulating fibrocytes were treated for 3 h and skin fibroblasts for 24/48 h with CTLA4-Ig (10, 50, 100, 500 μg/ml). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed for CD86, COL I, FN, TGFβ, αSMA, S100A4, CXCR2, CXCR4, CD11a, and Western blotting was performed for COL I and FN.

resultsUsing qRT-PCR, the T8-cultured SSc circulating fibrocytes which had not been treated with CTLA4-Ig showed higher gene expression for CD86, αSMA, S100A4, TGFβ, and COL I compared with HS circulating fibrocytes. Interestingly, αSMA/COL I gene expression was significantly lower only in the SSc circulating fibrocytes treated with CTLA4-Ig for 3 h (p < 0.01, p < 0.05). On the contrary, no effects were observed for either SSc or HS skin fibroblasts after CTLA4-Ig treatment. COL I and FN protein expression was unchanged in both SSc and HS skin fibroblasts by Western blot.

conclusionsCirculating fibrocytes seem to be more responsive to CTLA4-Ig treatment than skin fibroblasts from the same SSc patient, likely due to their higher expression of CD86. CTLA4-Ig treatment might downregulate the fibrotic process in SSc patients by downregulating the fibrocytes, circulating progenitor cells.

Indexed as

AbataceptAgedAntirheumatic AgentsBone Marrow CellsCells, CulturedFemaleFibroblastsHumansIn Vitro TechniquesMaleMiddle AgedScleroderma, SystemicSkinStem CellsAbataceptAntirheumatic AgentsConnective tissue diseaseCTLA4-IgFibrocytesSkin fibroblastsSystemic sclerosis

Identifiers

PMID30053831
PMCPMC6062881
OpenAlexW2884455125

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.