A2.19 The Role of microRNA 155 in Innate Immunity and Arthritis. (25th February 2013)

• Record Type: Journal Article
• Authors: Saferding, Victoria; Goncalves-Alves, Eliana; Puchner, Antonia; Smolen, Josef; Redlich, Kurt; Blüml, Stephan
• Is Part Of: Annals of the rheumatic diseases. Volume 72:Supplement 1(2013)
• Page Start: A11
• Page End: A11
• Publication Date: 2013-02-25
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2013-203215.19
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: MicroRNA 155 (miR155) has been demonstrated to be essential for the development of collagen induced arthritis by controlling the generation of autoreactive T and B cells. However, the contribution of miR155 in innate immune cells is not known. Materials and Methods: We analysed activation and cytokine production of macrophages and dendritic cells (DCs) in vitro and in vivo. We analysed T-cells stimulatory capacity of DCs. We crossed miR155 deficient mice into hTNFtg mice and analysed arthritis development clinically as well as histologically. Results: MiR155 deficiency did not alter the expression of costimulatory molecules or MHCII expression after stimulation of macrophages and DCs in vitro and in vivo. We also Facs-sorted DCs after stimulation with LPS in vivo and determined the production of proinflammatory cytokines such as IL-23, IL-6 as well as TNF. We did not detect differences between wt and miR155 -/- mice. In addition, the T cell stimulatory capacity of wt and miR155 -/- was identical. When we analysed hTNFtg/miR155 -/- mice compared to wt mice, we did not detect differences in the clinical signs and symptoms of arthritis. Histologically, we even found slightly increased synovial inflammation in hTNFtg/miR155 -/- mice compared to wt mice. Conclusions: In contrast to the pivotal role of miR155 in autoimmunity requiring the adaptive immune system, the role of miR155 in innate immunity seems to be limited. This is emphasised by the fact that miR155 hardly influences the course of TNF-driven arthritis, which is mainly dependent on components of the innate immune system.