Cyclosporin

Cyclosporin A (CsA), a fungal metabolite used in therapeutic immunosuppression for the prevention of human organ transplant rejection, has been found to produce autoimmunity in both rodents and humans (Holladay and Smialowicz 2000). Women who received CsA during their pregnancies often delivered prematurely or had babies that were small-for-gestational-age (SGA) and had birth defects (cataracts, cleft palate, dysmorphic facial appearance, and so on). CsA has been found to prevent activation of CD8+ cytotoxic T-cell precursors by interfering with selective events during critical periods in thymocyte differentiation and clonal deletion. CsA also interferes with deletion of autoreactive T-cells after bone marrow reconstitution which in turn induces a variety of autoimmune responses in adult rodents. After exposure to CsA, fetal thymic organ cultures demonstrated that mature T-cell generation was completely blocked. These studies support the concept that the fetal immune system could be targeted by maternal dosing with CsA (Holladay and Luster 1994). Newborn mice after prenatal and postnatal CsA treatments were also found to display impaired thymocyte differentiation along with an absence of mature T cells in lymph nodes and spleen, and a lack of T cell function. Concluding evidence also predicts that CsA given prenatally may affect the same target organs in the embryo as in the adult and may further cause autoimmune disease later in the life of gestationally exposed individuals (Holladay and Smialowicz 2000).

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Free Yourself from Panic Attacks

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