Related Researcher

Author's Photo

Do, Yoonkyung
DC-based Immune System & Immunotherapy (DISNI) Lab
Research Interests
  • Study on various subsets of dendritic cells and their immunological functions
  • Vaccine development by targeting pathogenic antigens to distinct DC subsets via anti-DC-subset-specific-receptor monoclonal antibodies
  • Characterization of roles of DCs in tumor microenvironment and tumor metastasis
  • Studies on role of DCs in neuro-related diseases
  • Study DCs in collaboration with Biotechnology or Engineering field


Role of death receptor pathway in estradiol-induced T-cell apoptosis in vivo

Cited 25 times inthomson ciCited 25 times inthomson ci
Role of death receptor pathway in estradiol-induced T-cell apoptosis in vivo
Do, YoonkyungRyu, SHNagarkatti, MNagarkatti, PS
Apoptosis; Estrogen; Fas; FasL; Immunotoxicity; Thymus
Issue Date
TOXICOLOGICAL SCIENCES, v.70, no.1, pp.63 - 72
In the current study we investigated the mechanism by which β-estradiol-17-valerate (E2) induces apoptosis in T cells. To this end, C57BL/6 wild-type (+/+), Fas-deficient (C57BL/6-lpr/lpr), and FasL-deficient (C57BL/6-gld/gld) mice were treated with various concentrations of E2, including 75, 25, 5, 1, or 0.1 mg/kg body weight or the vehicle. The thymi from these mice were harvested on days 1, 4, or 7 following treatment, and cellularity and apoptosis were determined. Treatment with E2 caused a decrease in thymic cellularity at all doses except 0.1 mg/kg in all three groups of mice, particularly on days 4 and 7. Interestingly, however, the degree of thymic atrophy in C57BL/6-lpr/lpr and C57BL/6-gld/gld mice was significantly less than that seen in C57BL/6 wild-type mice. When thymocytes were analyzed for apoptosis, cells from C57BL/6-lpr/lpr and C57BL/6-gld/gld mice showed decreased levels of apoptosis. Moreover, cDNA array analysis of gene expression revealed that treatment with E2 upregulated several genes involved in apoptosis, including FasL, caspases, TRAIL, and iNOS, but not bcl-2 gene family. Reverse transcriptase-polymerase chain reaction data also demonstrated the increased expression of Fas and FasL genes following E2 treatment. Caspase 8 inhibitor blocked the E2-induced apoptosis of thymocytes in vitro. These data suggested that E2 may induce apoptosis by activating the death-receptor rather than the mitochondrial pathway. E2 treatment decreased the expansion of peripheral Vβ3+ T cells to the bacterial superantigen SEA in vivo and their subsequent in vitro proliferative response to SEA, thereby suggesting increased induction of apoptosis in Vβ3+ T cells. The current study suggests that E2 may trigger the death receptor pathway in vivo in T cells, thereby inducing apoptosis.
Go to Link
Appears in Collections:
BME_Journal Papers
Files in This Item:
2-s2.0-0036850414.pdf Download

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record


  • mendeley


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.