MURINE EXPERIMENTAL AUTOIMMUNE OOPHORITIS DEVELOPS INDEPENDENTLY OF GONADOTROPIN STIMULATION AND IS PRIMARILY LOCALIZED IN THE STROMA AND THECA

PROBLEM: Neonatal thymectomy performed on day 3 of life (NTX3) induces experimental autoimmune oophoritis in certain strains of mice. The di sease has its onset around the time of the first estrous, suggesting t he process may be gonadotropin dependent. Furthermore, one study repor ted that gonadotropin stimulation exacerbated the ovarian lymphocytic infiltration in NTX3 mice. Here we examine the possibility that gonado tropin ii stimulation of the ovary plays a role in the development of post-thymectomy autoimmune oophoritis. METHOD: Using immunohistochemis try we defined the time course and histologic distribution of the post -thymectomy ovarian lymphocytic infiltration that develops in B6A mice ([C57BL6 X A/J]F-I). We detected ovarian leukocytes using a monoclona l antibody against mouse CD45/T200 and counted those positive staining cells that had the morphologic appearance of lymphocytes. We then tre ated NTX3 mice to determine if gonadotropin stimulation could exacerba te the disease or cause the disease to appear earlier. We also treated NTX3 mice to determine if gonadotropin suppression could reduce the s everity of the disease. RESULTS: Ovarian lymphocytic infiltration was observed as early as 3 weeks after thymectomy, and, during the course of the disease, was primarily located in the stroma and theca. Gonadot ropin stimulation did nor exacerbate existing disease or induce an ear lier onset of severe disease. Furthermore, gonadotropin suppression di d not reduce the degree of lymphocytic infiltration or oocyte destruct ion. CONCLUSIONS: Our findings suggest that murine experimental autoim mune oophoritis develops independently of gonadotropin stimulation of the ovary.