Fig. 3From: IKKβ deletion from CNS macrophages increases neuronal excitability and accelerates the onset of EAE, while from peripheral macrophages reduces disease severityKnocking out IKKβ selectively from CNS macrophages results in earlier onset and exacerbated chronic EAE. A–C Comparison of EAE between IKKβF/F and ΜgΙΚΚβΚΟ mice that was induced at 5 days after tamoxifen (4 doses), when IKKβ was depleted from both CNS and peripheral myeloid cells. A Representation of the mean EAE clinical score over 30 days post-immunization with the peptide MOG35-55. B Mantel Cox graph showing the proportion (%) of asymptomatic IKKβF/F and ΜgΙΚΚβΚΟ animals over 25 days post immunization with the peptide MOG35-55. C Comparison of the mean day of EAE onset between the IKKβF/F and ΜgΙΚΚβΚΟ mice. D–F Comparison of EAE between IKKβF/F and ΜgΙΚΚβΚΟ mice that was induced at 28 days after tamoxifen (2 doses), when IKKβ was depleted only from CNS myeloid cells. A Representation of the mean EAE clinical score over 30 days post-immunization with the peptide MOG35-55. B Mantel Cox graph showing the proportion (%) of asymptomatic IKKβF/F and ΜgΙΚΚβΚΟ animals over 25 days post immunization with the peptide MOG35-55. C Comparison of the mean day of EAE onset between the IKKβF/F and ΜgΙΚΚβΚΟ mice. Numbers of mice are annotated as scatter dots on the bars. All mice were adult females 2–4 months oldBack to article page