Thymic atrophy via estrogen-induced apoptosis is related to Fas/FasL pathway

A convincing body of evidence indicates that estrogen has significant immunomodulatory properties, including induction of thymic involution. However, it is unclear whether or not estrogen induces thymic involution by triggering apoptosis depended on Fas-FasL interactions. In the present study, estradiol-17beta (E(2)) was used to treat rats by gavages at 10, 1, 0.1, 0.01, and 0 ng/kg/day, respectively. Atrophy of thymus was determined by in situ morphological examination. Apoptotic cells were identified by terminal deoxynucleotide transferase-mediated deoxy-UTP nick end labeling (TUNEL) assay. A semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method was used to analyze Fas and FasL mRNA levels. The results showed that E(2) induced thymic atrophy, increased the rates of apoptotic death, and enhanced the Fas/FasL mRNA levels. These findings suggested that Fas/FasL-mediated apoptosis involved in the induction of thymic atrophy by E(2).