title: [Maternal anti-paternal reactivity--depends on etiology].
abstract: 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.
authors.affiliation: Institut für Immunologie und Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald.
authors.forename: C
authors.initials: C
authors.lastname: Schütt
mesh_terms: D000026:Abortion, Habitual / Q000276:immunology*; D016207:Cytokines / Q000097:blood; D005260:Female; D005333:Fetus / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007231:Infant, Newborn; D007247:Infertility, Female / Q000276:immunology*; D008297:Male; D011247:Pregnancy; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines