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Page count: 124

Abstract: Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) thought to be initiated by myelin-specific CD4+ T cells. MS is characterized by inflammation that leads to the destruction of myelin as well as myelin-producing cells, oligodendrocytes, and axonal degeneration within the CNS. MS disease relapses are markedly reduced during pregnancy, with the greatest suppression in disease activity observed during the third trimester. A rebound in disease activity is observed following parturition, suggesting MS disease suppression is specific to the gestation period. In order to examine the mechanisms of disease suppression, we developed a model of T cell transfer using myelin oligodendrocyte glycoprotein-specific transgenic cells as the donor population. T cell encephalitogenicity was not altered during pregnancy; however, exosomes, small lipid-bound vesicles that function as facilitators of intercellular communication, were augmented in the serum of pregnant mice and have been implicated in feto-maternal tolerance. Exosomes are able to modulate the activity of cells in both the immune and central nervous systems by relaying molecular signals from their cell of origin to target cells. Therefore, we sought to elucidate the role of serum exosomes in pregnancy-associated MS suppression.