Abstract
Trypanosoma brucei is one of only a few unicellular pathogens that thrives extracellularly in the vertebrate host. Consequently, the cell surface plays a critical role in both immune recognition and immune evasion. The variant surface glycoprotein (VSG) coats the entire surface of the parasite and acts as a flexible shield to protect invariant proteins against immune recognition. Antigenic variation of the VSG coat is the major virulence mechanism of trypanosomes. In addition, incessant motility of the parasite contributes to its immune evasion, as the resulting fluid flow on the cell surface drags immunocomplexes toward the flagellar pocket, where they are internalized. The flagellar pocket is the sole site of endo- and exocytosis in this organism. After internalization, VSG is rapidly recycled back to the surface, whereas host antibodies are thought to be transported to the lysosome for degradation. For this essential step to work, effective machineries for both sorting and recycling of VSGs must have evolved in trypanosomes. Our understanding of the mechanisms behind VSG recycling and VSG secretion, is by far not complete. This review provides an overview of the trypanosome secretory and endosomal pathways. Longstanding questions are pinpointed that, with the advent of novel technologies, might be answered in the near future.
Highlights
African trypanosomes rely on efficient strategies of immune evasion to successfully establish and maintain an infection in both their insect and mammalian hosts (Pays et al, 2014)
We summarize the main aspects of the corresponding pathways in yeast and mammals first and subsequently highlight differences and gaps in our knowledge of the exo- and endocytosis machineries in T. brucei
In T. brucei, the mechanism of transport from the Golgi to the flagellar pocket (FP) remains elusive and it may be possible that different carriers, perhaps containing different cargos, are involved (Figure 1)
Summary
African trypanosomes rely on efficient strategies of immune evasion to successfully establish and maintain an infection in both their insect and mammalian hosts (Pays et al, 2014). While the cis-Golgi network receives cargo from the ER, the medial-Golgi cisternae contain glycosylation enzymes and process cargo proteins and lipids, and the trans-Golgi network (TGN) sorts cargo molecules for delivery to different destinations (e.g., to the cell surface or to vacuolar or lysosomal compartments) (reviewed in Di Martino et al, 2019; Huang and Wang, 2017). In T. brucei, the mechanism of transport from the Golgi to the FP remains elusive and it may be possible that different carriers, perhaps containing different cargos, are involved (Figure 1).
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