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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: IKKβ deletion from CNS macrophages increases neuronal excitability and accelerates the onset of EAE, while from peripheral macrophages reduces disease severity

Fig. 1

Global depletion of myeloid IKKβ results in slight earlier onset and significantly supressed chronic EAE. A Representation of the mean EAE clinical score for IKKβF/F and MφIKKβΚΟ female mice over 50 days post immunization with the peptide MOG35-55. B Table showing experimental parameters, such as incidence, mean day of onset, mortality rate and mean day of death, of the three different EAE experiments that took place in bone marrow chimeric groups that were generated from IKKβF/F (F/F) and mφIKKβΚΟ (KO) female mice. Specifically, MOG35-55-EAE was induced in two experimental groups of chimeric mice; (1) KO- > F/F with IKKβ depleted peripheral myeloid cells and IKKβF/F CNS macrophages, (2) F/F- > KO with IKKβF/F peripheral myeloid cells and IKKβ depleted CNS macrophages and in two controls; (1) KO- > KO with IKKβF/F depleted CNS macrophages and peripheral myeloid cells, and (2) F/F- > F/F with IKKβF/F CNS macrophages and peripheral myeloid cells. The F/F- > F/F group is not included in the table because only one mouse survived in this group and could not be statistically compared with the others. C, D Representation of the mean EAE clinical score for the chimeric group of mice F/F- > F/F, KO- > KO, KO- > F/F and F/F- > KO over 18 days post immunization with the peptide MOG35-55. E Comparison of the mean day of EAE onset between the chimeric group of mice KO- > F/F, KO- > KO and F/F- > KO. Numbers of mice are annotated as scatter dots on the bars. All mice were adult females 2–4 months old

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