[2019 Fall Life Sciences & IBB Seminar]
▶Subject: Significant Role of AngiogenicFactors in Autoimmunity beyond Angiogenesis
▶Speaker: Prof. Wan-Uk Kim (The Catholic University of Korea)
▶Date: 4:30PM/Nov. 22(Fri.)/2019
▶Place: Auditorium(1F), Postech Biotech Center
T-helper (Th) cells actively communicate with adjacent cells by secreting soluble mediators, and yet crosstalk between Thcells and endothelial cells is poorly understood. Here, we demonstrated that the placental growth factor (PlGF), an angiogenicfactor, was selectively secreted by Th17 cells, and promoted angiogenesis in vitro and in vivo. Interestingly, angio-lymphokinePlGF, in turn, specifically induced Th17 cell differentiation and plasticity by activating STAT3 via binding to the FLT1 and NRP1 receptors and substituted for IL6 activity in IL17 production, whereas it suppressed FOXP3+ Tregcell generation. The disruption of PlGFattenuated the severity of delayed-type hypersensitivity and experimental autoimmune encephalomyelitis in mice by reducing IL17 production; the adoptive transfer of PlGF-overexpressing CD4+ T cells to these mice restored their disease phenotypes. On the contrary, selective overexpression of PlGFin T cells increased disease severity and IL17 and STAT3 expressions in mice with autoimmune arthritis. Finally, we observed a correlation between concentrations of PlGFand IL17 in the synovial fluids and synovial CD4+ T cells of rheumatoid arthritis patients. Conclusively, our findings provide novel insights into the PlGF-dictated links between angiogenesis, Th17 cell development, and autoimmunity, indicating that PlGFinhibitors could be used to control autoimmune and inflammatory diseases in hope of dual inhibition of angiogenesis and Th17 cell generation.
▶Inquiry: Prof. Sung Ho Ryu (279-2292)