Neonatal Autoimmune Ovarian Disease

To investigate autoAb without concomitant T cell response, we studied a chimeric peptide (CP) that contains the foreign T cell epitope of bovine ribonuclease (94-104) and the ZP3 (335-342) native B cell epitope. The peptide (CP2) elicited strong epitope-specific Abs that bound to the ovarian ZP in vivo. Despite this, the adult ovaries were free of pathology (Lou et al. 1995). The only observable effect in adult mice was the retargeting the location of ZP3-specific Th1 or Th2-mediated tissue destruction from the ovarian interstitium to the ovarian follicles (Lou et al. 2000).

Unexpectedly, over 80% of the progenies from the ZP3-positive dams developed severe nAOD at 2 weeks of age, and 40% of those with nAOD developed ovarian atrophy, premature ovarian failure and infertility (Setiady et al. 2003) (Fig. 3). Severe nAOD was induced by serum or purified serum IgG from adult female or male mice immunized with CP2 in CFA, or by transfer of a mouse monoclonal Ab to ZP3 (335-342). Therefore, autoAb to the ZP3 (335-342) B cell epitope is sufficient to trigger severe and frequent nAOD, a process independent of maternal lymphocytes or pregnancy-associated factors.

Fig. 3A-C The pathology of nAOD. A Normal ovary of a 2-week-old mouse, with numerous growing ovarian follicles. B Atrophic ovary in severe nAOD shows loss of all oocytes. C Ovarian inflammation has replaced the oocyte of an ovarian follicle in nAOD. (H&E; A, X50; B, X75; C, X400)
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100 Pregnancy Tips

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