dale1994's version from 2016-05-05 13:03


Question Answer
HLA-C:KIR interactions?-these interaction induce strong dNK inhibition -increase liklihood of pree in which trophoblast invasion and vascular remodelling are impaired -critical in regulation of placentation -leads to variation in weight accross the population -inhibitor-small and activator-big -epigenetic mechanism for a more robust population
HLA-G and NK cells?non-polymorphic class, membrance bound -interact with a variet of receptors to suppress NK cell acticity -protection of foetus rendering cells resist to lysis by NK cells -secretion of cytokines and angiogenic factios by uterine NK cells -reduced expression in preganancy loss
Th1/Th2?Bias to Th2 important but IFN important
Reg T cells?CD4+CD25bright Tregs important -migrate from maternal peripheral blood to decidual tissue and suppress local immune response through TGF-b and IL-10
CD8 T cells?-largest population of Tcells at interface -possibly respond to foetal HLA-C -do not express perforin and do not elicit a fill cytotoxic response -
Progesterone?-Produced in grams per day, locally high concentration that act via its own and cortisol receptors as immunosuppressive -progesterone receptors upregulated on NK in decidua -PIBF which induces asymmetric Ab production, prevents effector functions, phagocytosis, complement activation, ADCC
PIBF increases?-Th2 cytokines IL-3, IL-4 and IL-10 -reduces IL-12 -inhibits NK cytotoxicity
GdAGlycodelin A -induced apoptosis of T cells -induces Th1 cell death -shifts ratio of Th1/Th2 response
HCG-immunosuppressive -important signal for cytotrophoblasts to become invasive in transplantation -indicator of early pregnancy failure
IDO-depletes tryptophan in trophoblast vicinity -T cells affected -remains available to foetus -decreases in early pregnancy (shrockshnadel 1996)
Complement Inhibitors?-CD46 membrane co factor protein -CD55 decay accelerating factor -CD59 membrane inhibitor of reactive lysis

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