1 accines and case reports of human autoimmune oophoritis.

2 lts in the failure to induce both autoimmune oophoritis and autoantibody production.

3 evealed that Aod1 controls susceptibility to oophoritis and comprises two linked QTL with opposing al

4  the ovary tissue revealed the occurrence of oophoritis and reduced growth of the ovary in herbicide-

5 ction of noninfectious ovarian inflammation (oophoritis) and serum antibody to ovarian and placental

6 es, antiovarian autoantibody responsiveness, oophoritis, and atrophy, to five quantitative trait loci

7 e development of antiovarian autoantibodies, oophoritis, and atrophy.

8                                 AOD began as oophoritis at 3 wk.

9                  Mice with amAb often had no oophoritis; but more importantly, bilateral ovariectomy

10 e detectable ZP3 T cell response (day 5) and oophoritis (day 7) failed to prevent the amAb response,

11    A ZP3 peptide contains both an autoimmune oophoritis-inducing T cell epitope and a B cell epitope

12 hibin-alpha-targeted experimental autoimmune oophoritis is initiated by CD4(+) Th1 T cells that stimu

13 s diseases including hearing loss, orchitis, oophoritis, mastitis, and pancreatitis.

14 ng phenomenon based on the murine autoimmune oophoritis model.

15 k, ovaries engrafted at 5 wk had more severe oophoritis than ovaries engrafted at 6 or 12 wk; moreove

16 symptoms of mumps together with orchitis and oophoritis that can arise in males and females, respecti

17 cates in cells of the ovary and causes acute oophoritis, there is rapid resolution and no long-term e

18 rferon gamma in vitro, were able to transfer oophoritis to normal recipients.

19 al follicles, and the resultant interstitial oophoritis was associated with unimpaired ovarian functi

20             The mice OX at 2 wk did not have oophoritis whereas approximately 80% of mice OX at 3 or

21  T cells and induces experimental autoimmune oophoritis with a unique biphasic phenotype characterize