Parasite immune evasion articles from across Nature Portfolio

Upon skin infection with the parasite Leishmania major, a small group of infected cells remain present in healed skin. Here, Zayats et al. show that regulatory T cells focused towards parasite-derived proteins have strong suppressive capabilities and facilitate parasite persistence in vivo.

The use of single cell sequencing has enabled more detailed analysis of the immune response to infection. Here the authors characterise the immune response to malaria infection in an endemic region using single cell transcriptomics indicating regulatory signatures associated with infection.

Antigenic variation is used by pathogens to evade the host immune system. This Review describes the impact of nuclear organization on antigenic variation in protozoan parasites.

Malaria parasites use various molecular tactics to hijack IgM antibodies and escape the human immune system.

Antigenic variation in protozoan parasites is considered a spontaneous process and antibodies to these variant antigens were cytotoxic. The clearance of the former antigen during antigenic switching is thought to occur by dilution of the original antigen. In this work, the authors provide in vitro and in vivo evidence, that low concentrations of antibodies against Variant-specific Surface Proteins (VSPs) of the intestinal parasite Giardia lamblia are not cytotoxic but induce a robust stimulation of the switching process and the release of the former antigen into extracellular microvesicles. This process is mediated by antibody-induced clustering of VSPs into L_o-phase membrane microdomains through the raftophilic capability of the highly conserved transmembrane domain of the VSPs.

African Trypanosomes have developed elaborate immune evasion mechanisms. Here, the authors present the cryoelectron microscopy structures of a trypanosome surface receptor with human complement C3 and C3b, revealing several modes of complement interaction.

This month’s Under the Lens discusses how recent advances in understanding the spatial integration of transcription and splicing sites have shed light on the mechanism that ensures monogenic antigen expression in trypanosomes.

This study reveals that Toxoplasma gondii maintains a replicative niche in neutrophils by extending their longevity through inhibition of apoptosis. This effect occurs by upregulation of PCNA expression, resulting in inhibition of caspase cleavage and activation.

What evolutionary strategies are used by parasites to flourish for long periods within their mammalian hosts? These are questions that have been addressed by Pinger et al. in a recent study that identifies variable O-glycosylation as a novel immune-evasion mechanism employed by African trypanosomes.

Rodent malaria parasites establish chronic infections through the sequential expression of subsets of variant antigen-encoding genes, a process that surprisingly appears to be independent of adaptive immunity.

Parasite access to the central nervous system is a severe complication of infection. Toxoplasma gondii can achieve this by directly infecting, replicating in and lysing blood–brain barrier endothelial cells.