Evidence map›Paper›PMID 35020867›Full record

ArticleClinical and experimental immunology2022

miR-155-overexpressing monocytes resemble HLAhighISG15+ synovial tissue macrophages from patients with rheumatoid arthritis and induce polyfunctional CD4+ T-cell activation.

Anton M Olsson, Giovanni A M Povoleri, Domenico Somma, Michael L Ridley, Tatiana Rizou, Sylvine Lalnunhlimi, Lucy Macdonald, Megha Rajasekhar, Rocio T Martinez-Nunez, Mariola Kurowska-Stolarska and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. 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

11 authors at 4 institutions in 2 countries.

Anton M OlssonCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Giovanni A M PovoleriCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Domenico SommaInstitute of Infection, Immunity, and Inflammation, University of Glasgow, Glasgow, UK.
Michael L RidleyCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Tatiana RizouCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Sylvine LalnunhlimiCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Lucy MacdonaldInstitute of Infection, Immunity, and Inflammation, University of Glasgow, Glasgow, UK.
Megha RajasekharCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Rocio T Martinez-NunezDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Mariola Kurowska-StolarskaInstitute of Infection, Immunity, and Inflammation, University of Glasgow, Glasgow, UK.
Leonie S TaamsCentre for Inflammation Biology and Cancer Immunology, Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK.ORCID 0000-0002-9337-7194
King's College London · GBArthritis UK · GBThe University of Melbourne · AUUniversity of Glasgow · GB

Funding

Department of HealthVersus Arthritis 20960Versus Arthritis 21139Versus Arthritis 22072Versus Arthritis 22272
6 · The paper itself

Abstract

MicroRNAs (miRs) are known to regulate pro-inflammatory effector functions of myeloid cells, and miR dysregulation is implicated in rheumatoid arthritis (RA), a condition characterized by inflammation and destruction of the joints. We showed previously that miR-155 is increased in myeloid cells in RA and induces pro-inflammatory activation of monocytes and macrophages; however, its role at the interface between innate and adaptive immunity was not defined. Here, RNA-sequencing revealed that overexpression of miR-155 in healthy donor monocytes conferred a specific gene profile which bears similarities to that of RA synovial fluid-derived CD14+ cells and HLAhighISG15+ synovial tissue macrophages, both of which are characterized by antigen-presenting pathways. In line with this, monocytes in which miR-155 was overexpressed, displayed increased expression of HLA-DR and both co-stimulatory and co-inhibitory molecules, and induced activation of polyfunctional T cells. Together, these data underpin the notion that miR-155-driven myeloid cell activation in the synovium contributes not only to inflammation but may also influence the adaptive immune response.

Indexed as

Arthritis, RheumatoidMicroRNAsCD4-Positive T-LymphocytesHumansMacrophagesMonocytesSynovial MembraneMicroRNAsMIRN155 microRNA, humanIL-10immune regulationinnate immunitymicroRNAmonocyte

Identifiers

PMID35020867
PMCPMC8982969
OpenAlexW4205943951

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Registered trials

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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.