Virulent Toxoplasma gondii strain RH promotes T-cell-independent overproduction of proinflammatory cytokines IL12 and γ-interferon

Nguyễn, Tùng Lâm; Bigaignon, Geoffroy; Markine-Goriaynoff, Dominique; Heremans, Hubertine; Nguyen, Tran; Warnier, Guy; Delmée, Michel; Warny, Michel; Wolf, Stanley F.; Uyttenhove, Catherine; Snick, Jacques Van; Coutelier, Jean‐Paul

doi:10.1099/jmm.0.04860-0

Cited by 37 publications

(17 citation statements)

References 46 publications

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“…Our results showed that the kinetics of all three cytokines was remarkably similar in mice infected with either strain. Interestingly, while the levels of IL-10 elicited by infection with both BGD1 and ME49 strains were comparable with those obtained in the study of Mordue et al for experimental infection with a low inoculum of PTG parasites (a cloned line of ME49), the levels of IFN-g and IL-12 were by two and three orders of magnitude, respectively, lower in our experimental model than in this and other studies [17,19,24]. This may be associated with the murine host genotype.…”

Section: Discussionsupporting

confidence: 78%

A human origin type II strain of Toxoplasma gondii causing severe encephalitis in mice

Djurković–Djaković

Klun

Khan

et al. 2006

Microbes and Infection

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Section: Discussionsupporting

confidence: 78%

A human origin type II strain of Toxoplasma gondii causing severe encephalitis in mice

Djurković–Djaković

Klun

Khan

et al. 2006

Microbes and Infection

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“…This latter finding parallels the frequent paucity of this isotype in the autoantibodies of many (but not all) SLE models (48). Normally, IgG1 is the most prominent T-dependent IgG subclass against soluble protein Ags, although viruses and bacteria can provoke T-dependent, IgG2a-skewed responses (40,41). A similar outcome was observed in BAFF-transgenic mice that were completely deficient in T cells.…”

Section: Discussionsupporting

confidence: 55%

T Cell-Independent Spontaneous Loss of Tolerance by Anti-Double-Stranded DNA B Cells in C57BL/6 Mice

Tsao

Jiao

et al. 2008

The Journal of Immunology

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Systemic lupus erythematosus is characterized by loss of tolerance to DNA and other nuclear Ags. To understand the role of T cells in the breaking of tolerance, an anti-DNA site-specific transgenic model of spontaneous lupus, B6.56R, was studied. T cells were eliminated by crossing B6.56R with CD4−/− or TCRβ−/−δ−/− mice, and the effects on anti-dsDNA serum levels, numbers of anti-dsDNA Ab-secreting cells, and isotypes of anti-dsDNA were analyzed. In addition, the development and activation of B cells in these mice were examined. Surprisingly, the presence of T cells made little difference in the development and character of the serum anti-dsDNA Ab in B6.56R mice. At 1 mo of age, anti-dsDNA Abs were somewhat lower in mice deficient in αβ and γδ T cells. Levels of Abs later were not affected by T cells, nor was autoantibody class switching. B cell activation was somewhat diminished in T cell-deficient mice. Thus, in the B6 background, the presence of an anti-dsDNA transgene led the production of autoantibodies with a specificity and isotype characteristic of murine systemic lupus erythematosus with little influence from T cells. TLR9 also did not appear to play a role. Although we do not yet understand the mechanism of this failure of immunoregulation, these results suggest that similar processes may influence autoimmunity associated with clinical disease.

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“…In addtion, lamina propria CD4 + T-lymphocytes produce increased quantities of IFN-γ and TNF-α and participate in the host defense [10,11]. To stop parasite multiplication and to prevent host death due to T. gondii infection, IL-12 and IFN-γ are required [12]. …”

Section: Introductionmentioning

confidence: 99%

Immune Responses of Mice Intraduodenally Infected withToxoplasma gondiiKI-1 Tachyzoites

et al. 2011

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Toxoplasma gondii Korean isolate (KI-1) tachyzoites were inoculated intraduodenally to BALB/c mice using a silicon tube, and the course of infection and immune responses of mice were studied. Whereas control mice, that were infected intraperitoneally, died within day 7 post-infection (PI), the intraduodenally infected mice survived until day 9 PI (infection with 1×105 tachyzoites) or day 11 PI (with 1×106 tachyzoites). Based on histopathologic (Giemsa stain) and PCR (B1 gene) studies, it was suggested that tachyzoites, after entering the small intestine, invaded into endothelial cells, divided there, and propagated to other organs. PCR appeared to be more sensitive than histopathology to detect infected organs and tissues. The organisms spread over multiple organs by day 6 PI. However, proliferative responses of splenocytes and mesenteric lymph node (MLN) cells in response to con A or Toxoplasma lysate antigen decreased significantly, suggesting immunosuppression. Splenic CD4+ and CD8+ T-lymphocytes showed decreases in number until day 9 PI, whereas IFN-γ and IL-10 decreased slightly at day 6 PI and returned to normal levels by day 9 PI. No TNF-α was detected throughout the experimental period. The results showed that intraduodenal infection with KI-1 tachyzoites was successful but did not elicit significant mucosal immunity in mice and allowed dissemination of T. gondii organisms to systemic organs. The immunosuppression of mice included reduced lymphoproliferative responses to splenocytes and MLN cells to mitogen and low production of cytokines, such as IFN-γ, TNF-α, and IL-10, in response to T. gondii infection.

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Virulent Toxoplasma gondii strain RH promotes T-cell-independent overproduction of proinflammatory cytokines IL12 and γ-interferon

Cited by 37 publications

References 46 publications

A human origin type II strain of Toxoplasma gondii causing severe encephalitis in mice

A human origin type II strain of Toxoplasma gondii causing severe encephalitis in mice

T Cell-Independent Spontaneous Loss of Tolerance by Anti-Double-Stranded DNA B Cells in C57BL/6 Mice

Immune Responses of Mice Intraduodenally Infected withToxoplasma gondiiKI-1 Tachyzoites

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