University thesis:
Dissertation, Universitätsmedizin der Universität Greifswald, 2021
Footnote:
Literaturverzeichnis: Seite 66-74
Zusammenfassung in deutscher Sprache
Description:
B1-a B Cells, Preeclampsia
In this work we investigated immunological mechanisms involved in the onset of PE, a multifactorial pregnancy related disease of global importance. The clinical symptoms range from de novo hypertension, renal and hepatic damage, to IUGR and convulsions (eclampsia). An imbalance between vasospastic and vasodilatory mediators, leading to generalized endothelial dysfunction, is most probable responsible for the onset of the disorder. Autoimmune reactions provoked by the semi-allogen fetus have also been postulated as a possible cause. Preterm delivery is the only curative therapie available. Our focus was on a subset of B lymphocytes, the CD19+ CD5+ B1-a B cells. These cells belong to the innate immune system and produce natural polyreactive (and possibly autoreactive) antibodies such as AT1-AA but also different cytokines. In the context of PE it has been reported that B1-a B cells in the peripheral blood are augmented. Female sex hormones, pregnancy associated hCG and its isoform h-HCG modulate the immune functions in pregnancy and thus may be involved in the development of PE. Cytokine production patterns of B1-a B cells and the impact of female sex hormones were analyzed. For our experiments an established mouse model for immunological pregnancy loss (CBA/J x DBA/2J model) was used. Aditionally, isolated human peripheral blood B1-a B cells were used. In the mouse model we could demonstrate that in vivo transferred B1-a B cells induced deposits in the mothers’ kidneys, ...