In RA patients, an increased expression of miR-155 in monocytes/macrophages could be responsible for impaired maturation of monocytes into M2 anti-inflammatory macrophages. Our aim is to assess if the defect of M2 polarization and the impact of miR-155 and others microRNA in this defect are present in 2 pre-clinical models of RA: the CIA and STIA mice.
Project LeadA Paoletti
To demonstrate in mice model of rheumatoid arthritis (RA) that microRNA could be responsible of polarization of monocytes in pro-inflammatory macrophages in order to find a new safe treatment of RA specific of these cells.
microRNA inhibition by another molecule is already in progress in some cancer with an apparent good safety profile. If we confirm efficacy and specificity of our treatment in mice models of arthritis, this approach could emerge as a novel and possible treatment for rheumatoid arthritis patients. Moreover our therapeutic strategy uses a new way for addressing the possible new drug directly in the macrophages infiltrating the joints and thus, should be devoid of side effects