Background: In chronic PTSD, a preattentive neural alarm system responds rapidly to emotional information, leading to increased prefrontal cortex (PFC) activation at early processing stages (<100 ms). Enhanced PFC responses are followed by a reduction in occipito-temporal activity during later processing stages. However, it remains unknown if this neuronal pattern is a result of a long lasting mental disorder or if it represents changes in brain function as direct consequences of severe trauma.
View Article and Find Full Text PDFProblem: Indoleamine 2,3-dioxygenase (IDO) expression in fetal trophoblast and decidual antigen-presenting cells has been proposed to inactivate maternal T cells and thereby prevent rejection of the "fetal allograft" in early pregnancy. Psychic stress has been proposed to cause miscarriages as well as infertility, at the same time in pregnancy when blockade of IDO causes loss, but the suggested mechanism of stress-triggered loss has been an increased ratio of pro-rejection Th1-type cytokines to anti-rejection Th2/3 cytokines. Could stress act by reducing IDO expression?
Methods: Using DBA/2-mated A/J mice where stress causes early pregnancy failure, we examined the role of stress in reducing IDO versus increasing Th1/Th2 ratio in deciduas.
Our understanding why a woman's immune system does not reject her histoincompatible fetus is still very limited. Distinct insights into the mechanisms involved in pregnancy maintenance may help us to prevent pregnancy complications, e.g.
View Article and Find Full Text PDFOne of the most remarkable immunological regulations is the maternal immune tolerance toward the fetal semiallograft during pregnancy, which has been referred to as immunity's pregnant pause. Rejection of the semiallogeneic trophoblast cells must be selectively inhibited and pathways presumably include Th2 cytokines unopposed by Th1 cytokines. Steroid hormones, including progesterone, have similar effects.
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