IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier

Table 3 Myeloid-specific ikkβ gene deletion ameliorates transferred EAE

Group	Incidence (%)	Mean day of onset (± SEM)	Maximal clinical score (± SEM)	Sun of clinical score (± SEM)	Mortality (%)
Wild type	5/5	7.4 ± 1.6	4.2 ± 0.7	43.7 ± 10.6	10
→Wild type	5/5	7.4 ± 1.6	4.2 ± 0.7	43.7 ± 10.6	10
Wild type	5/5	9.4 ± 0.2	3.6 ± 0.2	33.7 ± 2.1	0
→LysM-Cre/Ikkβ ^F/F	5/5	9.4 ± 0.2	3.6 ± 0.2	33.7 ± 2.1	0
LysM-Cre/Ikkβ ^F/F	5/5	13.6 ± 1.6*	0.7 ± 0.1**	7.5 ± 2.1**	0
→Wild type	5/5	13.6 ± 1.6*	0.7 ± 0.1**	7.5 ± 2.1**	0
LysM-Cre/Ikkβ ^F/F	5/5	11.6 ± 1.4	1.4 ± 0.2**	12.9 ± 1.8**	0
→LysM-Cre/Ikkβ ^F/F	5/5	11.6 ± 1.4	1.4 ± 0.2**	12.9 ± 1.8**	0

T cells were isolated from lymph nodes of WT or LysM-Cre/Ikkβ ^F/F donor 15–18 days after induction of active EAE and re-stimulated with MOG_35–55 peptide. Purified T cells (1 × 10⁷) were transferred i.v. into sub-lethally irradiated WT or LysM-Cre/Ikkβ ^F/F recipient mice. (ANOVA test; *p < 0.05 and **p < 0.01 versus WT → WT group)

ISSN: 1750-1326