[Maternal anti-paternal reactivity--depends on etiology]

Since TH1-cytokines compromise pregnancy and TH2-cytokines are produced at the maternal-fetal interface one can hypothesize that TH2-cytokines improve fetal survival. Cytotoxic T- or NK-cells are unable to recognize MHCI/II-negative trophoblast or become inactivated by HLA-G expression, respectively. Normal delivery at term might be assisted by a rapid reversal of the TH2 cytokine bias. Thus, the maternal immune state is most beneficial to reproductive fitness.