Background: Preeclampsia (PE), a significant pregnancy disorder, can be classified as early-onset (34 wks) and late-onset (>34 wks) subtypes according to the timing of disease presentation. Endothelial dys-function is a major contributor of PE development. Soluble endoglin (sENG), kwon to be substantially increased in PE circulation, is thought to sequester TGFβ ligands, inhibiting TGFβ signalling and causing endothelial dysfunction. However, sENG has very low affinity for TGFβ ligands and it remains unsolved whether sENG alone is responsible for TGFβ inhibition in PE. TGFβ ligands signal via their main type I and type II receptors (TGFβRI and TGFβRII respectively), with endoglin and TGFβ type III receptor acting as co-receptors. Aims: we investigated whether all these TGFβ receptors are present in soluble forms in normal pregnant serum, whether they are altered in PE, and whether they can (alone or in combination) inhibit the signalling of TGFβ1/2 ligands. Methods and Results: We detected by ELISA sENG and all other 3 soluble TGFβ receptors (sTGFβRI, sTGFβRII, sTGFβRIII) in normal pregnant serum. The sENG levels were elevated in both PE subtypes, however, the other 3 soluble TGFβ receptors were significantly increased only in early-onset PE. In an in vitro model, none of these soluble TGFβ receptors alone at the concentration seen in PE circulation affected the signalling of TGFβ1 or TGFβ2. However, when all four were present, both TGFβ1 and TGFβ2 action was significantly inhibited. Furthermore, removal of anyone of these 4 soluble TGFβ receptors reversed the inhibition of TGFβ1 action, however, removal of sTGFβRIII was necessary to alleviate the inhibition of TGFβ2 signalling. Conclusions: Multiple soluble TGFβ receptors are elevated in early-onset PE circulation. TGFβ signalling inhibition is more likely associated with early-onset PE. Removal of sTGFβRIII rather than sENG would alleviate the inhibition of both TGFβ1 and TGFβ2 signalling in PE.