Interleukin 17 inhibits progenitor cells in rheumatoid arthritis cartilage. Issue 2 (14th December 2015)

• Record Type: Journal Article
• Authors: Schminke, Boris; Trautmann, Sandra; Mai, Burkhard; Miosge, Nicolai; Blaschke, Sabine
• Is Part Of: European journal of immunology. Volume 46:Issue 2(2016)
• Page Start: 440
• Page End: 445
• Publication Date: 2015-12-14
• Subjects: Cartilage Chondrogenesis ⋅ Chondrogenic progenitor cells ⋅ Rheumatoid arthritis ⋅ Interleukin 17 (IL‐17); Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201545910
• Languages: English
• ISSNs: 0014-2980

Abstract

Abstract : Mesenchymal stem cells are known to exert immunomodulatory effects in inflammatory diseases. Immuneregulatory cells lead to progressive joint destruction in rheumatoid arthritis (RA). Proinflammatory cytokines, such as tumour necrosis factor α (TNF‐α) and interleukins (ILs) are the main players. Here, we studied progenitor cells from RA cartilage (RA‐CPCs) that are positive for IL‐17 receptors to determinate the effects of inflammation on their chondrogenic potenial. IL‐17A/F reduced the chondrogenic potential of these cells via the upregulation of RUNX2 protein and enhanced IL‐6 protein and MMP3 mRNA levels. Blocking antibodies against IL‐17 positively influenced their repair potential. Furthermore, treating the RA‐CPCs with the anti‐human IL‐17 antibody secukinumab or the anti‐TNF‐α antibody adalimumab reduced the proinflammatory IL‐6 protein level and positively influenced the secretion of anti‐inflammatory IL‐10 protein. Additionally, adalimumab and secukinumab in particular reduced RUNX2 protein to promote chondrogenesis. The amelioration of inflammation, particularly via IL‐17 antagonism, might be a new therapeutic approach for enhancing intrinsic cartilage repair mechanisms in RA patients.