Fig. 2: IRAK-M deficiency deteriorates neurobehavioral symptoms and pathological changes in the EAE model. | Cell Death & Disease

Fig. 2: IRAK-M deficiency deteriorates neurobehavioral symptoms and pathological changes in the EAE model.

From: IRAK-M suppresses the activation of microglial NLRP3 inflammasome and GSDMD-mediated pyroptosis through inhibiting IRAK1 phosphorylation during experimental autoimmune encephalomyelitis

Fig. 2

A Average clinical scores of IRAK-M−/− and WT EAE groups, respectively (n = 12 per group). B The variation of body weight of IRAK-M−/− and WT EAE groups, respectively (n = 12 per group). C Relative fold induction of IRAK-M mRNA in the development of WT EAE on day 10 and at peak disease compared to WT CFA on day 18 (n = 5, respectively). ***P < 0.001 compared to the WT CFA group. ###P < 0.001 compared to WT EAE on day 10. D Representative images of H&E staining (upper panels on the left show a 4 × 10 magnification of the whole spinal cord, scale bar: 500 µm; lower show a 10 × 10 magnification of the anterior median region, scale bar: 200 µm). The right panel shows the evaluation of infiltrating degree (n = 12 per group). E Representative images of LFB staining. The uncolored area in the anterior white matter indicates the area of axonal injury (upper panels on the left show a 4 × 10 magnification of the whole spinal cord, scale bar: 500 µm; lower show a 10 × 10 magnification of the anterior median region, scale bar: 200 µm). The right panel shows the evaluation of the demyelination degree (n = 12 per group). Results were normalized to GAPDH. All results were from three representative experiments. Data show the mean ± SEM and were analyzed by an unpaired t-test (A, B, D, E) or the Mann–Whitney U test (C). **P < 0.01; ***P < 0.001.

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