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Fig. 3 | Journal of Neuroinflammation

Fig. 3

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

Fig. 3

Knocking out IKKβ selectively from CNS macrophages results in earlier onset and exacerbated chronic EAE. AC 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. DF 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 old

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