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

Bo Anton Olsson, Giovanni Povoleri, Domenico Somma, Michael Ridley, Tatiana Rizou, Sylvine Lalnunhlimi, Lucy Macdonald, Megha Rajasekhar, Rocio Martinez Nunez, Mariola Kurowska-Stolarska, Leonie Taams*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

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 characterised 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 characterised 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.
Original languageEnglish
JournalClinical and Expentmental Immunology
Early online date30 Nov 2021
DOIs
Publication statusE-pub ahead of print - 30 Nov 2021

Keywords

  • microRNA
  • IL-10
  • innate immunity
  • immune regulation
  • monocyte

Fingerprint

Dive into the research topics of 'miR-155 overexpressing monocytes resemble HLAhighISG15+ synovial tissue macrophages from patients with rheumatoid arthritis and induce polyfunctional CD4+ T cell activation'. Together they form a unique fingerprint.

Cite this