The role of interleukin 10 in immune tolerance – lessons learnt from human pregnancy
TL;DRAbstract
Pregnancy requires that the maternal immune system tolerates the semi-allogeneic fetus and therefore represents an important model for the study of human immune tolerance. The current thesis explores the immunological processes during pregnancy, focusing specifically on innate and adaptive immune interactions at the fetal-maternal interface and the transplacental regulation of maternal and fetal immunity. A unique population of DC-SIGN+ decidual antigen presenting cells (APCs) was identified, which efficiently induces Foxp3+ regulatory T (Treg) cells and CD4+HLA-G+ suppressive T cells. This process was shown to be defective in pre-eclampsia, in which a reduction of both induced Treg cells and CD4+HLA-G+ suppressive T cells was demonstrated. This immune tolerance breakdown likely contributes to the pathogenesis of pre-eclampsia. Interleukin 10 (IL-10) was identified as an important mediator of this fetal-maternal immune tolerance, where it was shown to tolerize APCs, upregulate HLA-G ex
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Pregnancy requires that the maternal immune system tolerates the semi-allogeneic fetus and therefore represents an important model for the study of human immune tolerance. The current thesis explores the immunological processes during pregnancy, focusing specifically on innate and adaptive immune interactions at the fetal-maternal interface and the transplacental regulation of maternal and fetal immunity. A unique population of DC-SIGN+ decidual antigen presenting cells (APCs) was identified, which efficiently induces Foxp3+ regulatory T (Treg) cells and CD4+HLA-G+ suppressive T cells. This process was shown to be defective in pre-eclampsia, in which a reduction of both induced Treg cells and CD4+HLA-G+ suppressive T cells was demonstrated. This immune tolerance breakdown likely contributes to the pathogenesis of pre-eclampsia. Interleukin 10 (IL-10) was identified as an important mediator of this fetal-maternal immune tolerance, where it was shown to tolerize APCs, upregulate HLA-G ex
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