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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Sema4A is implicated in the acceleration of Th17 cell-mediated neuroinflammation in the effector phase

Fig. 1

Adoptively transferred Th17, but not Th1, encephalitogenic cells exacerbate EAE in Sema4A-deficient mice. After active immunization, Sema4A KO (4AKO) mice exhibited less severe EAE clinical course than wild type (WT) mice (a). Either Th1- or Th17-skewed MOG-specific T cells were adoptively transferred to either WT or Sema4A KO mice (b). No significant difference was observed among the mice transferred with Th1-skewed WT MOG-specific encephalitogenic T cells (b, left panel). Sema4A KO mice receiving Th17-skewed WT MOG-specific encephalitogenic T cells showed a significant reduction in the clinical score (b, right panel). Infiltration of mononuclear cells in the spinal cord of Sema4A KO recipient mice was markedly attenuated when Th17-skewed WT MOG-specific encephalitogenic T cells were transferred (c). Data are expressed as means ± SEM. *P < 0.05. Scale bars, 300 μm

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