ANAMNESTIC DEVELOPMENT OF LYMPHOCYTIC INFILTRATION IN MURINE EXPERIMENTAL AUTOIMMUNE OOPHORITIS LS PRIMARILY LOCALIZED IN THE STROMA AND THECA

Citation
S. Raj et al., ANAMNESTIC DEVELOPMENT OF LYMPHOCYTIC INFILTRATION IN MURINE EXPERIMENTAL AUTOIMMUNE OOPHORITIS LS PRIMARILY LOCALIZED IN THE STROMA AND THECA, American journal of reproductive immunology [1989], 34(2), 1995, pp. 125-131
Citations number
23
Categorie Soggetti
Reproductive Biology",Immunology
ISSN journal
10467408
Volume
34
Issue
2
Year of publication
1995
Pages
125 - 131
Database
ISI
SICI code
1046-7408(1995)34:2<125:ADOLII>2.0.ZU;2-N
Abstract
PROBLEM: Neonatal thymectomy performed on day 3 of life (NTX3) induces autoimmune oophoritis and ovarian failure in B6A mice. These mice dev elop high-titer autoantibodies specific to oocytes, and ultimately the ovaries become fibrotic and devoid of primordial follicles. These fin dings implicate the oocyte as a primary target of the autoimmune proce ss. However, in previous work we demonstrated that in developing disea se the lymphocytic infiltration was confined to the stroma and theca, and not found involving oocytes. Here, we investigate the possibility that lymphocytic infiltration involving oocytes develops as part of en d-stage disease. METHOD: We transplanted normal syngeneic ovaries to : B6A mice with confirmed autoimmune ovarian failure, and, as a control, to normal oophorectomized mice. We then defined the time course and h istologic distribution of lymphocytic infiltration in the transplanted ovaries. Lymphocytes were identified by morphology with the aid of an immunohistochemical leukocyte marker (CD45). RESULTS: Autoimmune ooph oritis developed by 7 days after transplantation to the NTX3 mice. Com pared to control mice, in these mice we found significantly increased stromal and thecal lymphocytic infiltration. In no case did we observe lymphocytic infiltration involving oocytes. CONCLUSIONS: Our findings agree with our previous report and suggest that the ovarian failure i n this model is not mediated by a direct lymphocytic attack against in tact oocytes. Other immune-mediated mechanisms are responsible. The pa radoxical development of high-titer oocyte-specific antibodies despite the stromal and thecal location of the lymphocytic infiltration remai ns to be explained.