Invited Faculty
  • Sang-il Lee
    Gyeongsang Nat'l Univ.
  • In addition to various immune cells, several stromal cells including fibroblast-like synoviocytes (FLS), lymph node fibro-reticular cells (LN-FRC), and mesenchymal stem/stromal cells (MSC) have been implicated in the pathophysiology of rheumatoid arthritis (RA). Contrary to their protective roles in healthy condition, these stromal cells exhibit dysfunctional or aggressive properties influencing the activity of infiltrating immune and other tissue resident cells in autoimmune pathogenesis. Recently we have reported three important perturbations of stromal cells contributing to the immuno-pathogenesis and these results may provide directions for improving future therapy for RA. First, decreased Raf kinase inhibitory protein (RKIP) or phospholipase C-eta2 (PLCH2), which are negative regulators in upstream cellular signaling pathway, mediate the aggressiveness of RA-FLS and promote arthritic inflammation and the joint destruction. Second, T cell zone FRCs of LNs (LN-TRCs) express CD25, and CD25-deficient LN-TRCs promote T helper 17 (Th17) cell differentiation and Th17 response-related gene expression in Th17-dependent autoimmune diseases. Third, cellular senescence, due to a long-term exposure to the chronic inflammatory milieu, attenuated immunomodulatory properties of synovial fluid derived-MSC in a long-term RA. Thus, in this lecture, we will summarize recent progress on the molecular signature and the roles of stromal cells contributing pathological progression or presenting promising therapeutic tools for RA and extra-articular complications.
    Research & Clinical Focus

    Autoimmune diseases

    Rheumatoid arthritis

    Stromal cells

    Immune cells

  • Date Time Room Session Title Lecture Title
    May 18 10:30-11:00 Room Grand Ballroom 104+105 [Symposium] Year in Review Basic Interaction between stromal cells and immune cells: past, present, and future