| First Author | Derer A | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 8 | Pages | e101954 |
| PubMed ID | 25111378 | Mgi Jnum | J:218989 |
| Mgi Id | MGI:5619225 | Doi | 10.1371/journal.pone.0101954 |
| Citation | Derer A, et al. (2014) Blockade of IL-36 receptor signaling does not prevent from TNF-induced arthritis. PLoS One 9(8):e101954 |
| abstractText | INTRODUCTION: Interleukin (IL)-36alpha is a newly described member of the IL-1 cytokine family with a known inflammatory and pathogenic function in psoriasis. Recently, we could demonstrate that the receptor (IL-36R), its ligand IL-36alpha and its antagonist IL-36Ra are expressed in synovial tissue of arthritis patients. Furthermore, IL-36alpha induces MAP-kinase and NFkappaB signaling in human synovial fibroblasts with subsequent expression and secretion of pro-inflammatory cytokines. METHODS: To understand the pathomechanism of IL-36 dependent inflammation, we investigated the biological impact of IL-36alpha signaling in the hTNFtg mouse. Also the impact on osteoclastogenesis by IL-36alpha was tested in murine and human osteoclast assays. RESULTS: Diseased mice showed an increased expression of IL-36R and IL-36alpha in inflamed knee joints compared to wildtype controls. However, preventively treating mice with an IL-36R blocking antibody led to no changes in clinical onset and pattern of disease. Furthermore, blockade of IL-36 signaling did not change histological signs of TNF-induced arthritis. Additionally, no alteration on bone homeostasis was observed in ex vivo murine and human osteoclast differentiation assays. CONCLUSION: Thus we conclude that IL-36alpha does not affect the development of inflammatory arthritis. |
