. 2021 Oct;72:13–20. doi: 10.1016/j.coi.2021.02.007

Table 1.

Mechanisms allowing African trypanosomes to evade host immunity

	Host defence components	Parasite response
Specific innate immunity	- Human serum toxin (APOL1) targeted to the parasite through different Trojan horse strategies (VSG and TbHpHbR) [10^••,11, 12, 13]	- APOL1 neutralization (T. rhodesiense SRA) [8]; - Resistance to APOL1 (T. gambiense TgsGP) [21]
	- APOL1 C-terminal G1/G2 variants, which resist SRA of T. rhodesiense [22,24^••]	- Replacement of T. rhodesiense by T. gambiense in western Africa [11]
	- APOL3 nonsense variant, relieving APOL3-mediated G1/G2 inactivation [26,24^••]
General innate immunity	- Neutrophil DNA traps	- DNA cleavage (TatD DNases) [28] - Parasite motility (flagellum) [29]
	- Germline IgMs	- High membrane fluidity ensuring fast clearance of IgM-VSG complexes (TbKIFC1) [30^••]
	- Inflammatory response (TNF-α, NO, IL-1β, IL-6)	- Inhibition of early TNF-α synthesis (adenylate cyclases) [32] - NO synthase inhibition (TbKHC1) [34] - IL-1β/IL-6 inhibition (indole pyruvate) [35,36]
Adaptive immunity	- Anti-VSG IgGs	- High membrane fluidity ensuring fast clearance of IgG-VSG complexes (TbKIFC1) [30^••] - VSG antigenic variation (VEX1/VEX2: expression site selection; ATR: expression site switching) [44^••,45^••,55^••]
Adaptive immunity	- Antibodies against invariant surface receptors	- Receptor embedding within the VSG coat [3,61^•] - Receptor saturation shielding the ligand site - N-glycan coating - Antigenic variation of surface-exposed regions [63]