Metastatic lymph node 51 and fibroblast-like synoviocyte hyperproliferation in rheumatoid arthritis pathogenesis
- First Online:
- Cite this article as:
- Lim, DS. & Bae, YS. Rheumatol Int (2011) 31: 843. doi:10.1007/s00296-011-1818-x
- 178 Downloads
One of the varied characteristic features of the pathogenesis of rheumatoid arthritis (RA) is synovial hyperplasia. Fibroblast-like synoviocytes (FLSs) play a key role in the development of sustained inflammation in arthritic joints. We have reported previously that metastatic lymph node 51 (MLN51) is involved in the proliferation of FLSs in the pathogenesis of RA. Interestingly, the overexpression of MLN51 was observed only in RA FLSs, but not in osteoarthritis FLSs, possibly expecting that MLN51 may be a RA-specific marker. Additionally, we found that granulocyte–macrophage colony-stimulating factor signaling activates mitogen-activated protein kinase, followed by the upregulation of MLN51 and FLICE-inhibitory protein, resulting in FLS hyperplasia in RA. Based on these studies, we could be firm that MLN51 is a key factor in FLS hyperplasia of RA patients.