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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Interleukin-36γ is expressed by neutrophils and can activate microglia, but has no role in experimental autoimmune encephalomyelitis

Fig. 4

Neither IL-36γ nor IL-36R is required for EAE development. a Kaplan-Meier curves showing EAE incidence in mice expressing (black squares) or lacking (white squares) IL-36γ (upper graph) or IL-36R (bottom graph) after immunization with MOG. The graphs include all the mice tested. No significant intergenotype difference was detected (Wilcoxon tests, P ≥ 0.41). Sample size: 20 (IL-36γ+/+), 20 (IL-36γ−/−), 6 (IL-36R+/+), or 6 (IL-36R−/−). b EAE severity in mice expressing (black squares) or lacking (white squares) IL-36γ (upper graph) or IL-36R (bottom graph). The graphs include only mice that had developed clinical signs of EAE at the end of the study (i.e., 21 days). No significant intergenotype difference was detected (Wilcoxon tests, P ≥ 0.12). Sample size: 17 (IL-36γ+/+), 17 (IL-36γ−/−), 5 (IL-36R+/+), or 5 (IL-36R−/−). c Additional statistics for EAE in mice expressing (+/+) or not (−/−)IL-36γ or IL-36R. No significant intergenotype difference was detected in any of these parameters (Wilcoxon tests, P ≥ 0.34). Sample size: 20 (IL-36γ+/+), 20 (IL-36γ−/−), 6 (IL-36R+/+), or 6 (IL-36R−/−)

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