Murine experimental autoimmune oophoritis develops independently of gonadotropin stimulation and is primarily localized in the stroma and theca.
OBJECTIVE
Neonatal thymectomy performed on day 3 of life (NTX3) induces experimental autoimmune oophoritis in certain strains of mice. The disease has its onset around the time of the first estrous, suggesting the process may be gonadotropin dependent. Furthermore, one study reported that gonadotropin stimulation exacerbated the ovarian lymphocytic infiltration in NTX3 mice. Here we examine the possibility that gonadotropin stimulation of the ovary plays a role in the development of post-thymectomy autoimmune oophoritis.


METHODS
Using immunohistochemistry we defined the time course and histologic distribution of the post-thymectomy ovarian lymphocytic infiltration that develops in B6A mice ([C57BL6 X A/J]F1). We detected ovarian leukocytes using a monoclonal antibody against mouse CD45/T200 and counted those positive staining cells that had the morphologic appearance of lymphocytes. We then treated NTX3 mice to determine if gonadotropin stimulation could exacerbate the disease or cause the disease to appear earlier. We also treated NTX3 mice to determine if gonadotropin suppression could reduce the severity 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. Gonadotropin stimulation did not exacerbate existing disease or induce an earlier onset of severe disease. Furthermore, gonadotropin suppression did not reduce the degree of lymphocytic infiltration or oocyte destruction.


CONCLUSIONS
Our findings suggest that murine experimental autoimmune oophoritis develops independently of gonadotropin stimulation of the ovary.
Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892, USA.
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Nair
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Mastorakos
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Raj
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Nelson
D000595:Amino Acid Sequence; D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D005260:Female; D006062:Gonadotropins / Q000037:antagonists & inhibitors / Q000276:immunology / Q000494:pharmacology*; D007150:Immunohistochemistry; D007166:Immunosuppressive Agents / Q000494:pharmacology; D008214:Lymphocytes / Q000276:immunology / Q000473:pathology; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D009842:Oligopeptides / Q000494:pharmacology; D009869:Oophoritis / Q000209:etiology* / Q000276:immunology; D009928:Organ Specificity / Q000276:immunology; D011247:Pregnancy; D017154:Stromal Cells / Q000276:immunology*; D013799:Theca Cells / Q000276:immunology*
D006062:Gonadotropins; D007166:Immunosuppressive Agents; D009842:Oligopeptides; C057022:iturelix