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- W2015448061 abstract "Clinical approach to prevent T1DM began with immunosuppressive agents which were limited by direct toxicity, over-immunosuppression, or lack of specificity. Monoclonal antibodies were tried with only limited success. With better understanding of T-cell receptor structure and antigen presentation by MHC molecules, we attempted to prevent the disease by inhibiting the initiation of a pathologic immune response instead of intervening at the effector phase. In experimental autoimmune thyroiditis (EAT) in guinea pigs, we demonstrated that anti-thyroglobulin antibodies were not cytotoxic but rather protective. To study possible protective effects of autoantibodies in NOD mice, 6 week old female mice were immunized with pancreatic islets with incomplete Freund's adjuvant. High titers of anti-insulin, anti-islet, anti beta-cell, and anti-peri-islet Schwann cell antibodies were induced. By 32 weeks, 92% of 37 unimmunized female mice developed diabetes, but only 21% of 42 immunized mice developed diabetes (p<0.001). The placental transfer of antibodies also decreased the incidence of diabetes in offspring. In adoptive transfer, 5 SCID NOD mice were primed with unimmunized splenocytes and 6 received pancreatic islet-immunized splenocytes. One week later, they received diabetogenic splenocytes. All controls developed diabetes between 5-7 weeks. Mice receiving sensitized splenocytes developed diabetes between 17-28 weeks which demonstrated a delay in diabetic onset (p<0.0019) and indicated regulatory cell functions. We have developed a novel strategy (autoimmunization) to prevent or delay the onset of cell-mediated autoimmune diseases such as T1DM. Hopefully, these first steps will translate into human models." @default.
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- W2015448061 date "2008-03-01" @default.
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- W2015448061 title "A Novel Strategy in Prevention and Delay of Type I Diabetes Mellitus (T1DM) Onset by Autoimmunization" @default.
- W2015448061 doi "https://doi.org/10.1016/j.jaci.2008.01.043" @default.
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