Superantigen overcomes resistance of IL‐6‐deficient mice towards MOG‐induced EAE by a TNFR1 controlled pathway

IL-6, IL-17 and STAT3: a holy trinity in auto-immunity?

“…Moreover, disease in the IL-6 -/-mice can be partially rescued by injection with IL-8, a chemo-attractant whose secretion by endothelial cells is induced by IL-6 in combination with sIL-6R (88). Finally, injection of superantigen (staphylococcal enterotoxin B) increased VCAM-1 expression in brain endothelium and partially reversed resistance of IL-6 -/-mice to EAE (95). In conclusion, IL-6 plays a fundamental role in the pathogenesis of autoimmune encephalomyelitis, both by stimulating an encephalitogenic T cell response and by establishing the local inflammatory response via the induction of chemokines and the activation of the endothelium, possibly also increasing the permeability of the blood-brain barrier (96).…”

A model of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice for the characterisation of intervention therapies

“…A half-point scoring scale was adopted as used in previous studies in order to accurately record the daily progression of disease through relapse and remission periods (Eugster et al, , 1999(Eugster et al, , 2001. This scale allows the evaluation of subtle changes in neuronal pathology.…”

Postinfectious encephalomyelitis

“…Peripheral stimulation may also occur from microbial superantigen activation of lymphocytes that include autoreactive T-cell clones. In a mouse model of EAE, superantigens isolated from Staphylococcus induced paralysis by directly stimulating Vβ8-expressing T cells specific for the myelin basic protein peptide Ac1-11 [59,60].…”