Figure 6
Figure 6. Effect of rIL-5 treatment on induction of inflammatory T-cell subtypes in EAN. RT-PCR of cauda equina nerves (n = 10/group; *P ≤ .05, **P ≤ .01) showed that rIL-5 treatment for 9 days after onset of EAN (■) reduced the mRNA for TCR-α (Tcr-α), indicating there were less T cells than in EAN controls (□; P < .05; n = 10/group), but enhanced foxp3 (P = .05) and Il-5rα (P < .015), consistent with infiltration of Tregs (n = 10 rat samples/group). There was reduced mRNA for Il-2 (**P < .001), a Th1 cytokine, and Il-17A (**P = .008), a Th17 cytokine, and of Tnf-α a macrophage cytokine (*P < .05), indicating reduced infiltration of these autoimmune effector cells. mRNA of Th2 cytokines Il-5 (P = .03) and Il-4 mRNA (P = .08) were similar or increased in rIL-5–treated animals, indicating sparing of Th2 compared with Th1 and Th17 cells. T-beta and Gata3 were not increased. In summary, there was enhanced Ts2-associated mRNA (Foxp3, Il-5rα, with similar Ifn-γ), whereas there was suppressed Th1 (Il-2, T-bet) and Th17 (Il-17A), and sparing of Th2 (Il-4, Il-5, Il-10) cytokines. RT-PCR of the popliteal lymph nodes draining the site of immunization showed treatment with IL-5 for 9 days after onset of EAN had less mRNA for Tcr-α (**P < .006) and Tcr-β (P < .001; data not shown) than controls (n = 10 rat samples/group). The reduced Tcr-α was consistent with the increased B-cell numbers because of the effects of rIL-5. There was more mRNA for Il-5rα (*P = .04), Foxp3 (P = .05), and Gata3 (P < .01) in the IL-5–treated animals compared with controls. There was no differences in mRNA levels for Il-2, Il-17A, Il-10, or T-bet, but mRNA for Tnf-α (**P < .002) and Il-5 (*P < .02) was reduced in the IL-5–treated animals. The increased Foxp3 and Il-5rα and unchanged Ifn-γ were consistent with the presence of Ts2 cells. There was no suppression of Th1 or Th17 responses and sparing of some but not all Th2 cytokines.

Effect of rIL-5 treatment on induction of inflammatory T-cell subtypes in EAN. RT-PCR of cauda equina nerves (n = 10/group; *P ≤ .05, **P ≤ .01) showed that rIL-5 treatment for 9 days after onset of EAN (■) reduced the mRNA for TCR-α (Tcr-α), indicating there were less T cells than in EAN controls (□; P < .05; n = 10/group), but enhanced foxp3 (P = .05) and Il-5rα (P < .015), consistent with infiltration of Tregs (n = 10 rat samples/group). There was reduced mRNA for Il-2 (**P < .001), a Th1 cytokine, and Il-17A (**P = .008), a Th17 cytokine, and of Tnf-α a macrophage cytokine (*P < .05), indicating reduced infiltration of these autoimmune effector cells. mRNA of Th2 cytokines Il-5 (P = .03) and Il-4 mRNA (P = .08) were similar or increased in rIL-5–treated animals, indicating sparing of Th2 compared with Th1 and Th17 cells. T-beta and Gata3 were not increased. In summary, there was enhanced Ts2-associated mRNA (Foxp3, Il-5rα, with similar Ifn-γ), whereas there was suppressed Th1 (Il-2, T-bet) and Th17 (Il-17A), and sparing of Th2 (Il-4, Il-5, Il-10) cytokines. RT-PCR of the popliteal lymph nodes draining the site of immunization showed treatment with IL-5 for 9 days after onset of EAN had less mRNA for Tcr-α (**P < .006) and Tcr-β (P < .001; data not shown) than controls (n = 10 rat samples/group). The reduced Tcr-α was consistent with the increased B-cell numbers because of the effects of rIL-5. There was more mRNA for Il-5rα (*P = .04), Foxp3 (P = .05), and Gata3 (P < .01) in the IL-5–treated animals compared with controls. There was no differences in mRNA levels for Il-2, Il-17A, Il-10, or T-bet, but mRNA for Tnf-α (**P < .002) and Il-5 (*P < .02) was reduced in the IL-5–treated animals. The increased Foxp3 and Il-5rα and unchanged Ifn-γ were consistent with the presence of Ts2 cells. There was no suppression of Th1 or Th17 responses and sparing of some but not all Th2 cytokines.

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