Article Figures & Data
Figures
- FIG 1
IL-17A-deficient mice are more susceptible than WT mice to T. gondii infection. Eight-week-old wild-type (WT) and IL-17A-deficient (IL-17A−/−) B6 mice were orally (p.o.) infected with 10 or 30 cysts of the T. gondii Fukaya strain, and their survival was monitored daily. (A) Percent survival of WT (n = 19) and IL-17A−/− (n = 20) mice infected with 10 cysts. (B) Percent survival of WT (n = 15) and IL-17A−/− (n = 17) mice infected with 30 cysts. Statistically significant differences between WT and IL-17A−/− mice were analyzed by the Kaplan-Meier method (log-rank test). *, P < 0.05; **, P < 0.01.
- FIG 2
T. gondii loads in mLNs and ileum during acute phase of infection. WT and IL-17A−/− B6 mice were p.o. infected with 10 or 30 cysts of the T. gondii Fukaya strain, and the T. gondii loads in the mLN (A) and ileum (B) were measured by determination of the level of T. gondii B1 mRNA expression at 1 week p.i. Each symbol denotes the result for one mouse. The mean ± SD for three to four mice used in each experimental group is shown beside the symbols. Representative data from three independent experiments are shown.
- FIG 3
Effects of IL-17A deficiency on cytokine expression by mLNs during the acute phase of infection. Lymphocytes from the mLNs of uninfected (uninf.) or infected (T. gondii-inf.) WT and IL-17A−/− B6 mice were stained for intracellular IFN-γ (A), IL-4 (B), or IL-17 (C). (D) An isotype control was also used for staining. Representative data from two independent experiments with two to three mice in each experimental group are shown. The numbers shown are the percentages of cells contained in each square (the mean number of IFN-γ-positive CD4+ cells ± SD from four to five mice in two independent experiments are shown in parentheses in panel A).
- FIG 4
Histopathology of the ileal mucosa at 1 week after T. gondii infection. The ileal mucosa isolated from B6 mice infected or not infected is shown as T. gondii (+) or T. gondii (−), respectively. Mucosal damage, including goblet cell depletion, is evident in both WT and IL17A−/− mice with T. gondii infection, as determined with hematoxylin and eosin stain (HE) (A and G) and AB-PAS stain (B and H). The T. gondii SAG1 antigen was detected in both T. gondii-infected WT and IL-17A−/− B6 mice, while infiltration of neutrophils was evident in WT mice but not IL-17A−/− mice, as determined by immunohistochemistry for the T. gondii SAG1 antigen (C and I) and myeloperoxidase (MPO) (D and J). (Panel C and I insets) Magnified images of T. gondii. Bars, 100 μm (L) and 10 μm (panel I inset).
- FIG 5
Effects of IL-17A deficiency on cytokine expression in the ileum. The relative levels of expression of mRNA for IFN-γ (Α), IL-4 (B), and IL-17 (C) in the ileum of uninfected or T. gondii-infected WT and IL-17A−/− B6 mice were comparatively measured at 1 week p.i. Each symbol denotes the result for one mouse. The mean ± SD for three to four mice per group is shown beside the symbols. Representative data from three independent experiments are shown. Statistically significant differences between groups were analyzed by Student's t test (*, P < 0.05; **, P < 0.01). Differences between infected mice and uninfected mice are also shown (#, P < 0.05; ##, P < 0.01).
- FIG 6
Influence of IL-17A deficiency on T. gondii HSP70 expression in the ileum. The level of expression of T.g.HSP70 mRNA was measured at 1 week p.i. The level of expression of both the ATP-binding (A) and the C-terminal (B) sites of T.g.HSP70 mRNA in the ileum of WT (n = 8) and IL-17A−/− (n = 8) B6 mice are shown. Each symbol denotes the result for one mouse. The mean ± SD for each experimental group is shown beside the symbols. Representative data from three independent experiments are shown. Statistically significant differences between groups were analyzed by Student's t test. **. P < 0.01.
- FIG 7
Influence of IL-17A treatment on T.g.HSP70 expression. WT and IL-17A−/− B6 mice were treated with rmIL-17A at a dose of 0.5 μg/mouse every other day from −2 to 6 days p.i. The levels of expression of the ATP-binding or C-terminal site of T.g.HSP70 mRNA in the ileum (A, E), mLN (B, F), liver (C, G), and spleen (D, H) were measured at 1 week p.i. Each symbol denotes the result for one mouse. The mean ± SD for three to six mice in each experimental group is shown beside the symbols. Representative data from three independent experiments are shown. Statistically significant differences between groups were analyzed by Student's t test. *, P < 0.05; **, P < 0.01.
- FIG 8
Effects of IL-17A treatment on IFN-γ expression. The levels of expression of IFN-γ mRNA in the ileum (A), mLN (B), liver (C), and spleen (D) from WT and IL-17A−/− B6 mice that were uninfected (uninf.), infected and treated with rmIL-17A at 0.5 μg/mouse (inf., rmIL-17A), or infected and not treated with rmIL-17A (inf.) were measured at 1 week p.i. Each symbol denotes the result for one mouse. The mean ± SD for three to six mice per group is shown beside symbols. Representative data from three independent experiments are shown. Statistically significant differences between groups were analyzed by Student's t test. *, P < 0.05; **, P < 0.01. The differences between uninfected and infected mice were statistically significant (P < 0.001) for both IL-17A-deficient and WT mice (A to D).
- FIG 9
Anaphylactic reaction in T. gondii-infected IL-17A-deficient mice. T. gondii-infected WT and IL-17A−/− B6 mice received rT.g.HSP70 i.p. at 1 week p.i., and the mice were monitored for clinical signs of an anaphylactic reaction every 30 min. (A) Rectal body temperature (squares) and changes in Ht levels (ΔHt; circles) of WT (open symbols) or IL-17−/− (closed symbols) mice. ΔHt was calculated as follows: [(value postchallenge − value prechallenge)/value prechallenge] × 100. (B) Peripheral platelet numbers per 1,000 RBCs of WT (white symbols) or IL-17A−/− (black symbols) mice counted before (circles) and 3 h after (squares) rT.g.HSP70 injection. Individual data points are shown with means ± SDs. (C) Total scores for clinical signs in WT (n = 13; open circles) and IL-17A−/− (n = 14; closed circles) mice. Each symbol denotes the result for one mouse. The mean ± SD for each experimental group is shown beside the symbols. (D) Relative levels of IFN-γ mRNA expression in the liver and spleen of WT and IL-17A−/− uninfected mice (uninf.), mice infected and treated with rT.g.HSP70 administration (inf., rT.g.HSP70), or mice infected and not treated with rT.g.HSP70 (inf.). Each symbol denotes the result for one mouse. The mean ± SD for three to four mice per group is shown beside the symbols. Representative data from three independent experiments are shown. Statistically significant differences between groups were analyzed by Student's t test. *, P < 0.05; **, P < 0.01.
- FIG 10
Effect of an anti-T.g.HSP70 antibody on the survival of IL-17A−/− mice during the acute phase. IL-17A−/− B6 mice infected with 30 T. gondii cysts were treated (n = 12; closed circles with a dotted line) or not treated (n = 12; closed circles with a solid line) with an anti-T.g.HSP70 MAb at days 5 to 11 p.i., and their survival was compared with that of infected WT mice (n = 12; open circles with a solid line). Statistically significant differences between untreated WT and IL-17A−/− mice were analyzed by the Kaplan-Meier method (log-rank test). *, P < 0.05.
