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Pregnancy and Murine Thyroiditis: Thyroglobulin Immunization Leads to Fetal Loss in Specific Allogeneic Pregnancies¹

Division of Endocrinology and Metabolism, Departments of Medicine (M.I., A.P., M.K., L.A., T.F.D.) and Pathology (P.U.), Mount Sinai School of Medicine, New York, New York 10029

Address all correspondence and requests for reprints to: Dr. T. F. Davies, Mount Sinai Medical Center, Box 1055, 1 Gustave L. Levy Place, New York, New York 10029. E-mail: terry.davies{at}mssm.edu

Thyroid autoantibodies are risk factors in human pregnancy. To investigate the influence of autoimmune thyroiditis on pregnancy, we have studied the impact of murine experimental autoimmune thyroiditis (EAT) on pregnancy outcome by using thyroglobulin (Tg) immunized CBA/J (H2^k) female mice. When Tg immunized mice were mated with BALB/c (H2^d) males, only 57% (47/83) of pregnant mice maintained their conceptions compared with >85% of other strain combinations (P < 0.05). We also found that MHC class II antigens were expressed on placental cells from Tg immunized pregnant mice but not in control normal pregnancies. Furthermore, the frequency and severity of thyroiditis, assessed by histological analyses, was also increased in Tg immunized mice mated with the BALB/c strain compared with syngeneic pregnancies (P < 0.05). In these pregnant mice mated with BALB/c, interleukin-4 secretion by mitogen-stimulated spleen cells was significantly suppressed and interferon- secretion by mixed lymphocyte reactions with BALB/c cells was significantly increased. These data demonstrated enhanced Th1 cell proliferation and fetal loss in CBA/J X BALB/c pregnancies. We concluded, therefore, that pregnancy loss was increased in experimental autoimmune thyroiditis in a manner that was dependent on paternal antigens. These observations have broad implications for understanding the immunology of pregnancy.

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