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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: GPR43 stimulation on TCRαβ+ intraepithelial colonic lymphocytes inhibits the recruitment of encephalitogenic T-cells into the central nervous system and attenuates the development of autoimmunity

Fig. 3

Colonic TCRαβ+ T-cells acquire an inflammatory profile upon EAE, which might be reverted by GPR43 stimulation. A IEL and B LPL were isolated from healthy (black) or EAE mice (red) at 15 dpi and then re-stimulated with PMA/Iono/BFA for 3 h to analyse the expression of pro- and anti-inflammatory surface molecules and cytokines in CD4+, CD8αα+ and CD8αβ+ TCRαβ+ T-cells. Values are the percentage of T-cells producing IL-17, IFNγ, IL-10 or expressing PD-1. Each symbol represents data obtained from an individual mouse. C and E IEL and D LPL were isolated from the colon of WT healthy mice and then ex vivo stimulated with PMA/Iono/BFA in the presence of 1.5 μM 4-CMTB (blue symbols), 100 μM Propionate (grey symbols) or left untreated (black symbols). F IEL were isolated from the colon of WT (open bars) or GPR43 knockout (KO; grey-filled bars) healthy mice and then ex vivo stimulated with PMA/Iono/BFA. Then intracellular cytokine staining was analysed by flow cytometry. Values are the percentage of T-cells producing IL-17, IFNγ, IL-10 or expressing PD-1. Each symbol represents data obtained from an individual mouse. AF Mean ± SD are indicated. Data were obtained from AB 3–8, CD 14, or EF 3–5 mice per group. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001 by paired (C and D) or unpaired (A, B and F) Student’s t-test, or by one-way ANOVA followed by Dunnett’s post-hoc test (E)

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