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Anamnestic Development of Lymphocytic Infiltration in Murine Experimental Autoimmune Oophoritis Is Primarily Localized in the Stroma and Theca
Author(s) -
RAJ SHAILAJA,
NAIR SHARMILA,
MASTORAKOS GEORGE,
NELSON LAWRENCE M.
Publication year - 1995
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.1995.tb00928.x
Subject(s) - theca , stromal cell , infiltration (hvac) , stroma , lymphocytic infiltration , oocyte , autoimmune disease , biology , thymectomy , immune system , immunology , follicle , endocrinology , medicine , pathology , antibody , immunohistochemistry , myasthenia gravis , embryo , microbiology and biotechnology , physics , thermodynamics
PROBLEM : Neonatal thymectomy performed on day 3 of life (NTX3) induces autoimmune oophoritis and ovarian failure in B6A mice. These mice develop high‐titer autoantibodies specific to oocytes, and ultimately the ovaries become fibrotic and devoid of primordial follicles. These findings implicate the oocyte as a primary target of the autoimmune process. However, in previous work we demonstrated that in developing disease 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 end‐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 histologic distribution of lymphocytic infiltration in the transplanted ovaries. Lymphocytes were identified by morphology with the aid of an immunohistochemical leukocyte marker (CD45). RESULTS : Autoimmune oophoritis developed by 7 days after transplantation to the NTX3 mice. Compared 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 in this model is not mediated by a direct lymphocytic attack against intact oocytes. Other immune‐mediated mechanisms are responsible. The paradoxical development of high‐titer oocyte‐specific antibodies despite the stromal and thecal location of the lymphocytic infiltration remains to be explained.