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Highlights • Preclampsia results from dysregulation of complement regulation • It is due to abnormal expression of embryonic complement regulatory proteins • This in turn causes a down regulation of Treg activity. Abstract In this summary of my presentation in the last Reunion workshop I discuss a few assertions on preeclampsia, then turn on a (not fully testable) model where an embryonic defect in expression of embryo/ placental regulatory proteins results in complement activation, itself responsible for a down regulation of the T regs activity, resulting in a very early lack of complete down regulation of the preimplantation decidual inflammation, causing in the post implantation stage a low grade but chronic inflammatory state. [ABSTRACT FROM AUTHOR]

Abstract: In this short remembrance paper, I survey (what I believe are) key events in the evolution of the concepts of preeclampsia from the first workshop in 1998 to the 2012 one, and from Tahiti to Reunion island, via Mauritius and Tioman Island. [Copyright &y& Elsevier]