Abstract
Murine cysticercosis by Taenia crassiceps is a model for human neurocysticercosis. Genetic and/or immune differences may underlie the higher susceptibility to infection in BALB/cAnN with respect to C57BL/6 mice. T regulatory cells (Tregs) could mediate the escape of T. crassiceps from the host immunity. This study is aimed to investigate the role of Tregs in T. crassiceps establishment in susceptible and non-susceptible mouse strains. Treg and effector cells were quantified in lymphoid organs before infection and 5, 30, 90, and 130 days post-infection. The proliferative response post-infection was characterized in vitro. The expression of regulatory and inflammatory molecules was assessed on days 5 and 30 post-infection. Depletion assays were performed to assess Treg functionality. Significantly higher Treg percentages were observed in BALB/cAnN mice, while increased percentages of activated CD127+ cells were found in C57BL/6 mice. The proliferative response was suppressed in susceptible mice, and Treg proliferation occurred only in susceptible mice. Treg-mediated suppression mechanisms may include IL-10 and TGFβ secretion, granzyme- and perforin-mediated cytolysis, metabolic disruption, and cell-to-cell contact. Tregs are functional in BALB/cAnN mice. Therefore Tregs could be allowing parasite establishment and survival in susceptible mice but could play a homeostatic role in non-susceptible strains.
Highlights
Murine intraperitoneal cysticercosis by Taenia crassiceps has been extensively used to study the influence of the host’s genetic background, sex factors, and immunity on the reproduction of infecting cysticerci
There are several examples of parasites profiting from host-derived molecules and resorting to evasion strategies to survive even in an immunologically specialized microenvironment like the central nervous system (CNS) (Adalid-Peralta et al, 2018)
We propose that T. crassiceps may promote the differentiation of regulatory T cells as a mechanism for immune evasion
Summary
Murine intraperitoneal cysticercosis by Taenia crassiceps has been extensively used to study the influence of the host’s genetic background, sex factors, and immunity on the reproduction of infecting cysticerci. Previous studies demonstrated that BALB/cAnN mice are more susceptible to parasite infection than C57BL/6 mice (Fragoso et al, 1996; Fragoso et al, 2008) Genetic differences between both mouse strains are widely documented, such as the background H-2 gene complex (Sciutto et al, 1991), the gene coding for the Qa-2 protein (Fragoso et al, 1996; Fragoso et al, 1998) and the locus called Tccr (T. crassiceps cysticercosis restrictive locus 1), associated to their distinctive phenotype (Ramirez-Aquino et al, 2011). Several strategies are used by cysticerci to evade the host immune response. Treg induction favors the establishment and survival of parasites like Heligmosomoides polygyrus (Grainger et al, 2010), Echinococcus multilocularis (Nono et al, 2020) and Plasmodium sp. (Hisaeda et al, 2004)
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