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Table 3 Myeloid-specific ikkβ gene deletion ameliorates transferred EAE

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

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
Wild type 5/5 9.4 ± 0.2 3.6 ± 0.2 33.7 ± 2.1 0
LysM-Cre/Ikkβ F/F
LysM-Cre/Ikkβ F/F 5/5 13.6 ± 1.6* 0.7 ± 0.1** 7.5 ± 2.1** 0
→Wild type
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
  1. 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 MOG35–55 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)