Germ Cell Apoptosis in Autoimmune Orchitis: Involvement of the Fas–FasL System
Article first published online: 7 JUL 2003
American Journal of Reproductive Immunology
Volume 50, Issue 2, pages 166–176, August 2003
How to Cite
Theas, S., Rival, C. and Lustig, L. (2003), Germ Cell Apoptosis in Autoimmune Orchitis: Involvement of the Fas–FasL System. American Journal of Reproductive Immunology, 50: 166–176. doi: 10.1034/j.1600-0897.2003.00074.x
- Issue published online: 7 JUL 2003
- Article first published online: 7 JUL 2003
- Submitted February 6, 2002; revised March 26, 2002; accepted April 02, 2002.
- autoimmune orchitis;
- Fas–FasL system;
- germ cell apoptosis;
PROBLEM: The aim of this study was to determine the mechanism of germ cell death in experimental autoimmune orchitis (EAO) and the involvement of the Fas–FasL system in this process.
METHOD OF STUDY: The EAO was induced in rats by immunization with testis homogenate and adjuvants. Apoptosis was studied by light microscopy, in situ end labeling of apoptotic DNA and DNA fragmentation techniques. Fas, FasL and caspase 3 expression was detected by immunohistochemistry.
RESULTS: In rats with orchitis the number of Fas+ and FasL+ apoptotic germ cells increased from day 50, when the lesion develops, to 150 days, and correlates with the degree of testicular damage. Most spermatocytes expressing Fas were apoptotic. Many Fas+ germ cells were also immunoreactive for FasL. Moreover, these cells also expressed caspase 3.
CONCLUSIONS: In rats with EAO germ cell death occurs through an apoptotic mechanism preceding germ cell sloughing. Immunohistochemical data suggest that the Fas–FasL system mediates germ cell apoptosis in an autocrine and/or paracrine way.