Research on murine autoimmune ovarian disease (AOD) models suggests that th
e following sequence of events operate in prevention and induction of AOD.
Potentially pathogenic T cells for oocyte antigens that exist in normal mic
e are kept in check by regulatory CD25(+) T cells. Oocyte-specific pathogen
ic T cells are activated when the regulation is lost, as after day 3 thymec
tomy, or when T cells are stimulated through molecular mimicry. Activated,
proinflammatory T cells induce interstitial ovarian inflammation without di
sruption in ovarian function. Activated T cells also help B cells that resp
ond to endogenous oocyte antigens, to produce oocyte autoantibodies of dive
rsified specificities. Autoantibodies, nonpathogenic in themselves, retarge
t T cell-mediated inflammation to ovarian follicles resulting in ovarian at
rophy and ovarian failure. Future studies should determine the applicabilit
y of these findings to human ovarian autoimmunity. (J Soc Gynecol Investig
2001;8:S49-S51) Copyright (C) 2001 by the Society for Gynecologic Investiga
tion.