Ebola virus infection leads to systemic inflammatory response and coagulation disorders. It´s soluble Glycoprotein sGP, which is secreted by infected cells, was suggested to play an important role in immunomodulation. This study aimed to investigate the influence of sGP on leucocyte apoptosis as one possible mechanism. After generation of a recombinant sGP, a Jurkat-T- cell-model was established. Cells were incubated with sGP for several time periods. FACS-analysis revealed neither an increase nor decrease of apoptosis. In order to investigate possible cross reactions between sGP and the three death ligands TNFa, TRAIL and FasL or their receptors, cells were incubated with the respective ligands plus sGP. While sGP had obviously no influence on FasL- and TRAIL-induced apoptosis, TNFa- modulated apoptosis was slightly enhanced. Taken together, these experiments indicate that sGP, in contrast to the speculated role, does not effect apoptosis of lymphocytes on its own. However, interactions between sGP and TNFa or its receptor might play a moderate role in the modulation of apoptosis. Since sGP was described to have a protective effect on endothelial barrier function, the tendency of sGP to modulate apoptosis of Jurkat cells lights a more complicated effect of sGP in Ebola virus pathogenesis.