Receptor activator of NF-κB ligand (RANKL) is an essential cytokine for osteoclast differentiation, activation and survival. T lymphocytes such as T₁₇ cells, a subset of T helper cells that produce IL-17, play an important role in rheumatoid arthritic bone resorption by producing inflammatory cytokines and RANKL. It has not yet been clearly elucidated how T cell activation induces RANKL expression. T cell receptor activation induces the activation of nuclear factor of activated T cell (NFAT) and expression of its target genes. In this study, we examined the role of NFAT in T cell activation- induced RANKL expression. EL-4, a murine T lymphocytic cell line, was used. When T cell activation was induced by phorbol 12-myristate 13-acetate (PMA) and ionomycin, RANKL expression increased in a time-dependent manner. In the presence of cyclosporin, an inhibitor of NFAT activation, this PMA/ionomycin‐induced RANKL expression was blocked. Overexpression of either NFATc1 or NFATc3 induced RANKL expression. Chromatin immunoprecipitation results demonstrated that PMA/ionomycin treatment induced the binding of NFATc1 and NFATc3 to the mouse RANKL gene promoter. These results suggest that NFATc1 and NFATc3 mediates T cell receptor activationinduced RANKL expression in T lymphocytes.

고준위폐기물 기준처분시스템의 건전성과 처분안전성의 실험적 검증에 필수적 시설인 지하처분연구시설이 한국원자력연구원 부지 내에 건설되었다. 지하처분연구시설의 부지조사 결과에 대해 기술하고, 이 부지에 건설될 지하처분연구시설의 설계, 인허가, 건설 과정과 건설된 시설의 개요에 대해 하였다. 또 지하처분연구시설에서 수행 중인 현장실험에 대해 소개하였다.