Cytokines and chemokines production by mononuclear cells from parturient women after stimulation with live Toxoplasma gondii

Rezende-Oliveira

Mediators of Inflammation

et al. 2014

This study aimed to measure the synthesis of Th1 and Th2 cytokines by mononuclear cells after culture with live T. gondii and identified Th17 (CD4+) and Tc17 (CD8+) cells in toxoplasma-seronegative and toxoplasma-seropositive parturient and nonpregnant women. Cytometric bead arrays were used to measure cytokine levels (IL-2, TNF-α, IFN-γ, IL-4, IL-5, and IL-10); immunophenotyping was used to characterize Th17 and Tc17 cells, and the cells were stained with antibodies against CD4+ and CD8+ T cells expressing IL-17. The addition of tachyzoites to cell cultures induced the synthesis of IL-5, IL-10, and TNF-α by cells from seronegative parturient women and of IL-5 and IL-10 by cells from seropositive, nonpregnant women. We observed a lower level of IL-17-expressing CD4+ and CD8+ T lymphocytes in cultures of cells from seronegative and seropositive parturient and nonpregnant women that were stimulated with tachyzoites, whereas analysis of the CD4+ and CD8+ T cell populations showed a higher level of CD4+ T cells compared with CD8+ T cells. These results suggest that the cytokine pattern and IL-17-expressing CD4+ and CD8+ T lymphocytes may have important roles in the inflammatory response to T. gondii, thus contributing to the maintenance of pregnancy and control of parasite invasion and replication.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

IL-17-Expressing CD4⁺and CD8⁺T Lymphocytes in Human Toxoplasmosis

Rezende-Oliveira

Mediators of Inflammation

et al. 2014

“…T. gondii strains with different virulence are known to infect decidual immune cell populations and the placenta, a prime anatomical location to alter immune responses at the maternal‐foetal interface . On the other hand, the immunomodulation during pregnancy may contribute to the development of an environment (dominated by Th2 and Treg cells) that facilitates the escape of T. gondii from the immune response, leading to increased maternal pathology or an increased likelihood of congenital transmission …”

Section: Effect Of T Gondii Infection On the Developing Placenta Dementioning

confidence: 99%

How does toxoplasmosis affect the maternal‐foetal immune interface and pregnancy?

Borges

Brito

et al. 2018

Parasite Immunology

Toxoplasma gondii is a zoonotic parasite which, depending on the geographical location, can infect between 10% and 90% of humans. Infection during pregnancy may result in congenital toxoplasmosis. The effects on the foetus vary depending on the stage of gestation in which primary maternal infection arises. A large body of research has focused on understanding immune response to toxoplasmosis, although few studies have addressed how it is affected by pregnancy or the pathological consequences of infection at the maternal-foetal interface. There is a lack of knowledge about how maternal immune cells, specifically macrophages, are modulated during infection and the resulting consequences for parasite control and pathology. Herein, we discuss the potential of T. gondii infection to affect the maternal-foetal interface and the potential of pregnancy to disrupt maternal immunity to T. gondii infection. K E Y W O R D Sactivated-macrophage, congenital toxoplasmosis, immunopathogenesis, maternal-foetal Interface, pregnancy, zoonosis

“…There was a great increase in the CD8 + T lymphocytes subsets percentage in the pSAG1/SAG3 and pSAG1/SAG3-CTXA 2 /B immunization mice group, with the ratio of CD4 + T-cells and CD8 + T-cell in mononuclear cells showing significant differences compared to the control and pSAG1 immunization mice. Both T-cell subsets are important sources of IFN-γ, more optimum protective CD8 + T cell responses depend on the ability of CD4 + T-cells to provide the growth factor IL-2 [28,29]. Herein, compared with multivalent DNA vaccine immunization, introduction of CTXA 2 /B further enhanced the Th1 cell-mediated immunity with higher levels of IFN-γ but low levels of IL-4.…”

Section: Discussionmentioning

confidence: 99%

Compound DNA vaccine encoding SAG1/ SAG3 with A2/B subunit of cholera toxin as a genetic adjuvant protects BALB/c mice against Toxoplasma gondii

et al. 2013

BackgroundIntracellular parasites, such as T. gondii, present a plurality of antigens because of the complexity of its life cycle. Compound DNA vaccines bring a new approach and hope for the treatment of toxoplasmosis. In this study, a DNA vaccine encoding two major surface antigens SAG1, SAG3 from T. gondii, with A2/B subunit of cholera toxin as a genetic adjuvant was constructed.MethodsBALB/c mice were immunized intramuscularly with PBS, pcDNA3.1, pSAG1, pSAG1/SAG3 and pSAG1/SAG3-CTXA2/B three times separately. Immunized mice were tested for IgG antibody and IFN-γ and IL-4 production by ELISA. The proliferation of T cells was measured by DNA synthesis assay and the lymphocyte subsets of spleen cells by flow cytometry. All the immunized mice were challenged with 103 highly virulent RH tachyzoites of Toxoplasma gondii intraperitoneally and the survival times were recorded.ResultsAn enhanced production of IgG antibodies, antigen-specific lymphocyte proliferation and IFN-γ production from splenic cells were induced in mice immunized with pSAG1/SAG3 compared to mice immunized with pSAG1 (P<0.05). Introduction of CTXA2/B further enhanced the Th1 cell-mediated immunity with higher levels of IFN-γ, lymphocyte proliferation activity and percentage of CD8+ T-cells. When challenged with lethal doses of T. gondii (1×103), all control mice (PBS and empty plasmid group) died within 6 days. Mice immunized with pSAG1 died within 8 days. While 20% and 40% survival rate were achieved from mice immunized with pSAG1/SAG3 and pSAG1/SAG3-CTXA2/B.ConclusionsThis study indicates the compound DNA vaccine encoding T. gondii antigens SAG1, SAG3 with CTXA2/B gene was a promising DNA vaccine candidate against toxoplasmosis, which could effectively enhance the humoral and cellular immune response and prolong survival time in vaccinated mice.