Rheumatology International

, Volume 31, Issue 7, pp 843–847

Metastatic lymph node 51 and fibroblast-like synoviocyte hyperproliferation in rheumatoid arthritis pathogenesis


DOI: 10.1007/s00296-011-1818-x

Cite this article as:
Lim, DS. & Bae, YS. Rheumatol Int (2011) 31: 843. doi:10.1007/s00296-011-1818-x


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.


MLN51Fibroblast-like synoviocyteRheumatoid arthritisGM-CSF

Copyright information

© Springer-Verlag 2011

Authors and Affiliations

  1. 1.Department of Applied Bioscience, Laboratory for Immune Cell-based TherapyCHA UniversityBundang-gu, SungnamKorea
  2. 2.Department of Biological ScienceSungkyunkwan UniversitySuwonKorea