By P. Ambroise-Thomas, E. Petersen (auth.), Pierre Ambroise-Thomas, Peter Eskild Petersen (eds.)
This publication relies at the adventure of an ecu community on Congenital Toxoplasmosis which affiliates greater than 50 ecu really expert facilities from 17 diferent eu nations. a few American colleagues top-of-the-line experts on this planet additionally collaborate to this publication which provides the latest information on congenital toxoplasmosis in epidemiology, biology, scientific signs, diagnostic, remedy and prevention.
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Extra info for Congenital toxoplasmosis: Scientific Background, Clinical Management and Control
Dendritic cells, mononuclear phagocytes, and Toxoplasma gondii infection In vitro studies of human dendritic cells demonstrated a potent IL-12 response to either live T. gondii or parasite antigens but only in the presence of previously T. gondii-exposed T cells . Contact between the T cell and dendritic cells was important for optimal IL-12 production and suggested the need for a receptor-ligand interaction in regulating the dendritic cells response. In murine models, this receptor is CD40 on dendritic cells, which is stimulated by the T cell ligand CD40L [54-56].
Gondii infection In humans, NK and LAK cells are activated by T. gondii (Fig. 1) [24, 25]. In response to IL-12, TNF-y, IL-15 and IL-1B produced by T. gondii-infected macrophages, NK cells produce large amounts of IFN-y. IFN-y (in conjunction with TNF-y) activates murine macrophage and monocyte effect or function by stimulating reactive nitrogen intermediates (RNI) and oxygen free radical killing and tryptophan starvation. In mice, control of both acute and chronic T. gondii infection is dependent on IFN-yas shown by increased susceptibility to infection in mice treated with anti-IFN-y antibody .
A number of factors are known to influence the various steps of the controlled invasion, characteristically those stimulating proliferation have no effect on migration and invasion and vice versa. Stimulants of extravillous trophoblast proliferation are: EGF (paracrine effect), transforming growth factor (TGF, autocrine), colony stimulating growth factor (CSF-l, auto and paracrine), vascular endothelial growth factor (VEGF-l, paracrine (macrophages)) and placenta growth factor PIGF (autocrine effect).