immunology grant proposal

Fetal Immune Response To Infection With Toxoplasmosa gondii Tom Repici Immunology 4200 11-21-98 ABSTRACT I will be addressing the possible immunological barriers that may be involved with challenge to infection of Toxoplasmosa gondii, the protozoan that causes toxoplasmosis. It is widely known that toxoplasmosis is a devastating disease, with often drastic consequences upon infection. In pregnant mothers, these consequences can be very horrid. Such effects are more felt by the unborn fetus than by the mother. These effects include abortion, premature birth, and severe growth retardation (Creasy et. al., 1994). Falkner et. al. have shown that the human fetus is capable of producing antibodies as early as ten weeks gestation time. We also know that antibodies to toxoplasmosis exist, which are of Ig G, Ig M, and, recently demonstrated, although in low levels, Ig E isotypes. These facts give rise to some questions regarding the bizarre reactions of the fetus, which should be more than protected enough from infection. Why is the fetus damaged, or even aborted from such a challenge, when it has the ability to produce antibodies? Are any of the antibodies produced specific for toxoplasmosis? Are the maternal antibodies that may exist to toxoplasmosis found in fetal serum (due to the passive immunity from mother to child), or are they blocked by some selection mechanism in the placenta? My objectives are to find out 1)if the placenta does in fact serve as an antibody sponge (Creasy et. al.), 2)if the fetus produces antibodies specific for toxoplasmosis, 3)if fetal antibodies specific for toxoplasmosis are found, what isotype they are (to determine if they might be of maternal origin, since Ig G readily crosses the placenta), 4)if the antibodies found have a high affinity for toxoplasmosis immunogen and are capable of eliciting an effective immune response. BACKGROUND AND SIGNIFICANCE …

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