FIG. 3.

Fundamental role of B lymphocytes in the pathogenesis of pre-eclampsia. In pre-eclamptic patients, activated B cells differentiate into plasma cells that secrete autoantibodies specific for the type 1 angiotensin receptor (AT₁ AutoAb). These antibodies stimulate production of NADPH oxidase in the trophoblast cells of the placenta. In addition, B lymphocytes acting as antigen-presenting cells (APCs) present processed antigen in the context of a class II major histocompatibility complex (MHC II) to the T cell receptor (TCR), activating the T cell. Activated T cells display heightened NADPH oxidase activity. Conversely, CD4⁺ T cells also potentiate B lymphocyte activation through the same MHC II↔TCR interaction in a process termed T cell-dependent B cell activation. Superoxide (O₂⁻) accumulating in the placenta causes vascular endothelial dysfunction resulting in decreased uterine blood flow and placental ischemia.