Effect of CD4+CD25+ regulatory T cells on the immune evasion of Schistosoma japonicum

Abstract

It has been known that parasites developed sophisticated strategies to escape from the host immune assault. More recently, one strategy to induce immune evasion involved CD4(+)CD25(+) regulatory T cells (Tregs). Mice were infected with Schistosoma japonicum cercariae and then injected intraperitoneally with anti-CD25 monoclonal antibody (anti-CD25 mAb). The results showed that the percentages of CD4(+)CD25(+) Tregs in mice were expanded by S. japonicum infection, and it could be partially blocked by anti-CD25 mAb. Worm burden in anti-CD25 mAb group (23.17 ± 6.94) was significantly lower than that in infected group (30.17 ± 5.85). The level of interferon gamma was increased with anti-CD25 mAb administration; meanwhile, lower concentration of interleukin 10 was observed in the same group. These results suggest that CD4(+)CD25(+) Tregs contribute to the escape of S. japonicum from the host immune responses, while anti-CD25 mAb can partially block CD4(+)CD25(+) Tregs and enhance the protective immunity to the parasite by Th1-type immune response.

Characterization of peripheral blood T lymphocyte subsets in Chinese rhesus macaques with repeated or long-term infection with Plasmodium cynomolgi

“…Treg cells participate in the control of overwhelming responses to infectious agents (Raghavan and Holmgren 2005;Belkaid et al 2006;Demengeot et al 2006;Suvas and Rouse 2006). Tregs were reported to be involved in the immune responses and the inhibition of the protective immunity to parasites (Tang et al 2011). In our study, Treg counts continued to increase during malaria infection, particularly in the long-term infection group, and they quickly reverted to preinfection levels after the parasite was eliminated or controlled (Fig.…”

Mice lack of LRG-47 display the attenuated outcome of infection with Schistosoma japonicum

“…We speculated that the effect of IFN-γ act on at least partly through LRG-47; thus, IFN-γ downstream signaling could be hindered to some extent due to the deficiency of LRG-47 so that the express of IFN-γ was fed back to reduce. Furthermore, high level of IL-10 and Treg cells might further inhibit proliferation of Th1 cells and synthesis of IFN-γ (Abath et al 2006;Tang et al 2011). Besides the cellular immunity, LRG-47 −/− mice also showed the attenuated antibody response and the similar pathway changes in splenic gene profiling as well as IFN-γ −/− mice we ever studied (Du et al 2011).…”

Inmunorregulación inducida por helmintos: una actualización

“…Algunos han propuesto que el desarrollo de inmunosupresión mediada por Treg es un mecanismo de evasión de la respuesta inmunológica que utiliza el parásito a favor de su supervivencia (18,19); no obstante, también hay evidencia acerca de la protección que confieren sobre el daño tisular que produce la respuesta inflamatoria en contra de la infección (20). Las personas con esquistosomiasis o filariasis que desarrollan una fuerte inmunosupresión Figura 1.…”