Géraldine De Muylder

TL;DR: The protozoan parasite Trypanosoma brucei is lysed by apolipoprotein L-I, a component of human high-density lipoprotein (HDL) particles that are also characterized by the presence of haptoglobin-related protein, which explains its ability to capture trypanolytic HDLs.

TL;DR: It is shown that early after infection, these parasites subvert the first line of innate host defense by inhibiting tumor necrosis factor-α synthesis in myeloid cells, which provides a long-sought function for the abundant and diverse adenylate cyclases in salivarian trypanosomes.

TL;DR: A kinesin heavy chain released by T. brucei induces IL-10 and arginase-1 through SIGN-R1 signaling in myeloid cells, which promotes early trypanosome growth and favors parasite settlement in the host.

TL;DR: Trypanosome-suppressive immunomodulating factor (TSIF) may represent a new parasite molecule with the potential to modulate the host immune network, whereby it could contribute to the inflammatory response required to control parasite growth and to the pathogenicity of African trypanosomiasis, including immunosuppression.

TL;DR: It is reported that arginase expression and activity were induced in macrophages during mouse infection by Trypanosoma musculi, a natural parasite of this host, and this orphan kinesin plays an important role in promoting trypanosome infection.