Abstract
Toxoplasma gondii is an exceptionally successful parasite that infects a very broad host range, including humans, across the globe. The outcome of infection differs remarkably between hosts, ranging from acute death to sterile infection. These differential disease patterns are strongly influenced by both host- and parasite-specific genetic factors. In this review, we discuss how the clinical outcome of toxoplasmosis varies between hosts and the role of different immune genes and parasite virulence factors, with a special emphasis on Toxoplasma-induced ileitis and encephalitis.
Highlights
Toxoplasma gondii is an obligate intracellular parasite and the causative agent of toxoplasmosis, a worldwide zoonotic disease that can affect virtually all mammals and birds, including approximately one third of humans (Montoya and Liesenfeld, 2004; Pappas et al, 2009)
Role of Inflammasomes in Sensing Parasites In mammals or mice lacking TLR11, activation of the immune system upon Toxoplasma infection is dependent on cytoplasmic sensors such as NLRP1/3, the adaptor protein apoptosis associated speck-like protein containing a caspase activating and recruitment domain (CARD) (ASC) and the caspases 1 and 4, all of which lead to the secretion of IL1β and IL18, a process known as inflammasome activation (Witola et al, 2011; Gov et al, 2013, 2017; Mukhopadhyay et al, 2020a)
It is likely that, besides TgWIP, ROP17 is important in type II and III strains to reach the brain or other distant organs (Lambert et al, 2009). In support of this possibility, a recent study showed that the formation of tissue cysts in the brain of infected mice is almost completely abrogated in the type II Pru rop17 strain, which had a decreased virulence (Fox et al, 2016). These results suggest that the integrin-dependent crossing of the blood-brain barrier (BBB) is not the main mechanism used for type II strains, as otherwise it would be expected that in the absence of ROP17 the parasite had an enhanced transmigration through the BBB
Summary
Toxoplasma gondii is an obligate intracellular parasite and the causative agent of toxoplasmosis, a worldwide zoonotic disease that can affect virtually all mammals and birds, including approximately one third of humans (Montoya and Liesenfeld, 2004; Pappas et al, 2009). There are important differences in how the innate immune system of different host species detect Toxoplasma and, once it is detected, how it is eliminated via IFNγ-induced anti-parasitic activities.
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