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Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease that preferentially affects women during their reproductive years. Previous studies have reported that children born to mothers with SLE display a higher incidence of learning disorders than children born to healthy mothers. Although the cause of this disparity is still unknown, maternal SLE antibodies have been proposed as a likely candidate. SLE is an autoimmune disease characterized by the production of autoantibodies (AAbs), many of which contribute to tissue injury. During SLE pregnancy, the developing fetus receives maternal lupus AAbs via the placenta. Supporting the maternal antibody hypothesis for the incidence of learning disorders in the children of mothers with SLE is the key observation that none of the children born to fathers with SLE exhibit learning disorders. This intriguing hypothesis, however, has not been examined experimentally. The goal of this thesis is to explore the maternal antibody-mediated fetal brain injury hypothesis and to determine the consequences of in utero exposure to maternal SLE AAbs on fetal brain development and long-term cognitive capacities of the offspring.
